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基因劣势与早年健美启蒙 主持人卢卡斯介绍乔尔·格林（Joel Greene），称赞其在功能性营养、减脂及免疫系统优化领域提供了极具原创性的见解。

探索人类健康优化的初衷

乔尔坦言这一切源于其糟糕的家族遗传基因：他的母亲一生饱受低血糖折磨并最终死于癌症，而患有糖尿病的父亲则死于相关的肾脏并发症。这种家庭背景使他从五岁起便在电视偶像杰克·拉兰内（Jack LaLanne）的影响下接触健身。到了七十年代，上小学四年级的乔尔赶上了当时的跑步狂热，开始绕着街区跑步，并惊奇地发现自己长出了股四头肌。为了提升50码短跑的速度，他在五年级时开始了每日冲刺跑训练。同时，在《世界体育报道》（Wide World of Sports）节目中目睹弗兰克·赞恩（Frank Zane）击败阿诺德·施瓦辛格（Arnold Schwarzenegger）赢得奥林匹亚先生的画面，深深激发了他对健美的痴迷。随后，他顺理成章地成为了高中和大学的田径及十项全能运动员。

代谢优化剂时代的极致减脂与摄食失调

进入九十年代初，健身界的营养手段从糊状的“代谢优化剂”（Metabolic optimizers）迎来了革命性的转变。斯科特·康利博士（Dr. Scott Conley）研发的MetRx粉剂横空出世，并在杰夫·埃弗森（Jeff Everson）、比尔·菲利普斯（Bill Phillips）以及首位产品代言人也门尼·梅萨（Yemeni Mesa）的推广下风靡一时。作为一名常去田径场冲刺的普通健身房常客，乔尔在使用MetRx后达到了前所未有的极低体脂率，实现了“瘦骨嶙峋”的极致拉丝状态。

然而，四五年后，他开始遭遇无法控制的暴食反弹。他后来才意识到，自己完全扰乱了控制食物摄入的激素分泌。在此之后，他陷入了漫长的试错期，尝试了纯生食、精确计算宏量营养素等各种饮食流派，但最终总是不可避免地重新囤积脂肪。

科技创业的高压与减重人群的顿悟

大约在2003年，乔尔转行进入科技行业，加入了一家初创公司。面对每天长达14小时的高压工作和层出不穷的业务危机，原本带着清晰腹肌入职的他，到2006年四十二岁时，体重暴增了三四十磅，达到了260磅。虽然肌肉量依然庞大，需要穿3X码的衬衫，但他变得臃肿且毫无耐力。

一个转折点发生在他与社区里一个16岁男孩摔跤时，仅仅一分钟他就彻底力竭。这种体能的崩塌促使他下定决心，要找到一种能在高压现实生活中生存下来的减脂方法。他随后创立了当时互联网上仅次于WebMD的第二大减肥网站，并在2007年发表了第一篇向大众科普肠道微生物组与体重下降关系的文章。他开发了一款无需计算热量的视觉化食物追踪软件，并通过企业健康项目，收集了超过一万五千名四五十岁久坐办公人群的数据。

面对台下成百上千名超重且无法进行体能训练的员工，乔尔顿悟：真正的减重方案必须是为那些身体已经“报废”、无法锻炼的人（就像因为身体损伤而只能卖减肥产品的橄榄球星丹·马里诺）设计的。这段经历以及后来在Quest Nutrition与创始人罗恩·佩纳（Ron Penna）等人的交流，促使他写出了第一本书《免疫代码》（The Immunity Code）。该书提出了一种通过特定细菌（嗜黏蛋白阿克曼菌与双歧杆菌家族）重塑年轻时期免疫系统的肠道方案。

极限冲刺作为抗衰的终极测试

主持人提及自己重新开始进行冲刺跑以降低体脂时，乔尔进一步阐释了这项运动在他生命中的核心地位。他讲述了自己在四十六岁生日时完成的一项名为“男子汉十项全能（Man-tathlon）”的严苛挑战：提着两个总重90磅的五加仑水桶，爬上1000英尺高的陡坡走完一英里，提着水桶下山后，紧接着进行一次毫无保留的200米全力冲刺。

乔尔在书中提出了一个后来被广泛引用的观点：无热身冲刺（No warmup sprinting）。他认为，无论生物学检测显示年轻了多少岁，如果不能像青少年那样在毫无防备的情况下随时爆发冲刺，就并不算年轻。去田径场连续跑六个耗时均低于30秒的200米冲刺，是人体所能承受的最艰难的训练，但在提升激素水平、改善情绪和削减脂肪方面无可替代。

蜂蜜中的松属素与还原论营养学的局限

乔尔近期发布的内容，提到的蜂蜜中天然存在的黄酮类化合物松属素（Pinocembrin）。乔尔表示，他新书《免疫代码饮食》（The Immunity Code Diet）的核心目的就是消除公众对诸如草酸盐、燕麦、蜂蜜等被各路饮食圈子妖魔化食物的误解。

他批评了将蜂蜜简化为单一“宏量营养素”或“碳水”的还原论观点。蜂蜜实际上是一个极其复杂的有机整体，不仅含有海藻糖等特殊糖类，其富含的松属素更是当今制药界的热门靶点。研究显示该黄酮类物质在抗癌、抗抑郁及抗炎方面潜力巨大，目前至少有三四十条药物研发管线与之相关。

乔尔指出，现代人正处于一种“语义思想控制”之中，极易被“它只是碳水”这种贴标签式的语汇遮蔽双眼，从而忽视了食物的全局生物学价值。

时间维度对饱和脂肪与内皮功能的影响

是否可以将这种批判性视角应用于多不饱和脂肪酸与饱和脂肪的争论？

乔尔抛出了一个被所有饮食部落忽视的核心变量：时间。，人体内存在积累、降解、代偿和衰减四种基本力量，这意味着同一种食物在生命的不同阶段会产生截然不同的效应。因此，必须摒弃非黑即白的二元对立思维。例如，二三十岁的年轻人可以毫无顾忌地摄入黄油和鸡蛋，但到了五十岁，随着血管状态的改变，同样的饱和脂肪可能演变为病理学灾难。

乔尔详细阐述了内皮细胞中的NOX酶（NADPH氧化酶）机制。这些酶是体内唯一已知产生自由基的酶，年轻时能精准调控自由基的产生，维持葡萄糖稳态并介导血管舒张。然而随着年龄增长，这些酶会走向失控，过度产生过氧化氢，干扰葡萄糖转运途径。与此同时，血管内起到类似汽车减震器作用的张力传感器——糖萼（Glycocalyx）也会退化衰减。当这两个机制失效时，饱和脂肪的处理方式会发生根本性改变，进而诱发心血管疾病。

乔尔强调，如果纯粹从实证出发，甚至可以为被极度妖魔化的菜籽油辩护（如改善血脂与血管状况），也可以拿草甘膦残留来反驳。但他认为这种争论掩盖了更大的真相：动植物食物之间存在深刻的协同作用，植物可以保护人体免受肉类毒性的侵害，而肉类则能填补植物营养的匮乏。

荤食肠道生态与肉类肽的血压调节机制

针对肉类中新发现的对代谢功能有益的肽类。乔尔指出，肉类中存在极具潜力的抗高血压肽（如APPV4），它们能够对血管紧张素转化酶（ACE）及肾素-血管紧张素系统产生极其有益的影响。考虑到后新冠时代ACE受体在整体代谢健康中的关键作用，这一发现尤为重要。乔尔明确表示，肉类是上消化道在各方面最理想的食物，而植物则是下消化道最理想的食物。如果采取极端的全荤食法，每天会有10到15克氨基酸溢出进入结肠。由于发酵氨基酸的细菌（如具核梭杆菌）多为促癌菌，这种单一饮食潜藏着巨大风险。而当饮食中混合了植物后，发酵的重心就会从蛋白质发酵菌转移到分解糖类的碳水发酵菌上，从而在保留肉类益处的同时屏蔽其负面影响。此外，健康离不开共生菌的协同：双歧杆菌深度参与肠道抗原感应及树突状细胞的摄取，而阿克曼菌则负责调节T细胞，两者的存活与繁衍高度依赖动植物结合的平衡膳食。

草酸解毒法则与口腔硝酸盐还原菌的绝对刚需

主持人提到为了避开草酸盐，已经将蔬菜摄入严格限制在胡萝卜、洋葱和白蘑菇，而避开了羽衣甘蓝和菠菜。

乔尔对此做出了强烈的回应，指出“草酸盐有害论”存在一个巨大的逻辑漏洞。旧观念错误地认为只有一种产甲酸草酸杆菌（O. formigenes）能降解草酸，但实际上肠道内有超过761种细菌（主要是乳酸杆菌和双歧杆菌等共生菌）构成了庞大的草酸解毒网络。在自然界的生存觅食中，人类往往只能吃到含有草酸的次优食物，但这恰恰刺激了肠道解毒菌群的繁衍。在一个呈现钟形曲线的人口分布中，只要肠道微生物组得到优化，处于中间94%标准差的绝大多数人适度摄入草酸食物并无大碍。

更致命的是，随着年龄增长，人体绝对刚需口腔中的硝酸盐还原菌，它们依靠饮食中的硝酸盐（正是来源于那些富含草酸的绿叶蔬菜）存活。如果缺乏这些细菌将硝酸盐转化为亚硝酸盐，人体将无法修复失控的NOX酶和退化的糖萼，进而彻底丧失维持心血管健康的能力。因此，一味回避这些蔬菜反而会剥夺人体解决更重大衰老问题的武器。

阿克曼菌的内源性氮偏好与天然GLP-1激动剂的构建

在回顾阿克曼菌（Akkermansia）的重要性时，乔尔指出这种细菌主要以肠道黏液层中的黏蛋白（糖蛋白）为食。虽然它在进食时会使黏液层变薄，但这反过来会激活相关基因，促使肠道分泌出更厚实、更强健的黏液层。它通过多种途径（如IgA和T细胞调节）与双歧杆菌协同优化免疫系统。极其独特的是，阿克曼菌偏好内源性氮（即黏液分泌物），而大量摄入饮食中的外源性氮（蛋白质）反而会抑制其种群数量。它在浆果中的酚类物质滋养下茁壮成长，并在人体处于乏食状态时繁衍。然而物极必反，过度的乏食或饥饿会导致阿克曼菌繁殖过剩，最终过度啃食并耗尽肠道黏膜。此外，阿克曼菌还是天然的GLP-1激动剂。

顺着GLP-1的话题，主持人提及当下用于抑制食欲的司美格鲁肽（Semaglutide）等药物热潮。

乔尔坦言，普通食物永远无法达到合成药物那样强大的半衰期与威力，但通过饮食靶向触发GLP-1与GIP（抑胃肽）依然是一项极具价值的技能。研究表明，在糖尿病患者中，GIP对血糖控制的影响甚至大于GLP-1。天然激活GLP-1的食物包括鸡蛋、蛋白质与肠道可发酵纤维的组合（例如牛排配土豆），以及蜂蜜与甜菊糖的协同作用。

乔尔在书中设计了一款强效GLP-1奶昔：将乳清蛋白（改善胰岛素功能并激活GLP-1）、坚果酱（脂肪激活GLP-1）、甜菊糖、蜂蜜以及抗性淀粉（与乳清蛋白结合可增加脂肪氧化）混合。他强调，进食顺序与时机同样至关重要，在正餐前20分钟摄入这种“预载（Preload）”餐，就能利用纯粹的食物在体内激发出最强大的GLP-1荷尔蒙反应。

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1. 关于“无热身冲刺作为抗衰终极测试”的运动生理学风险 乔尔主张将“能否在无热身状态下进行全力冲刺”作为检验生物学年龄的绝对金标准，这一观点虽然在修辞上极具煽动性且符合进化论中应对突发危机的逻辑，但在现代运动医学语境下极其危险。随着年龄增长，人体的肌腱、韧带、筋膜的胶原蛋白交联度增加，弹性和含水量必然下降。鼓励中老年人跨越热身阶段直接进行极限神经肌肉爆发力输出，极易导致跟腱断裂、腘绳肌撕裂乃至诱发急性心血管事件。这混淆了“保持年轻时的爆发力阈值”与“无视身体组织的物理老化规律”之间的界限。

2. “时间维度与内皮功能衰退”对饱和脂肪定性的降维打击 乔尔对饱和脂肪与多不饱和脂肪酸之争的拆解极为精妙。他引入的“NOX酶失控与糖萼退化”理论，拥有坚实的血管生物学基础。传统营养学往往试图找到一种绝对“有益”的宏量营养素，而乔尔指出，由于年龄增长导致的微观血管器质性改变（自由基泛滥与葡萄糖转运受损），原本安全的饱和脂肪会演变为病理学诱因。这种将代谢状态作为第一性原理的动态营养观，是对当今社交媒体上“生酮拥趸”和“反肉斗士”非黑即白教条的有力驳斥。然而，心血管疾病的病理发生不仅取决于内皮层，还受ApoB颗粒浓度、系统性炎症等多种变量影响，将饱和脂肪的威胁完全归结于内皮氧化应激略显简化。

3. 对“草酸盐妖魔化”的微生物学反向工程 针对保罗·萨拉迪诺等极端荤食倡导者引发的“草酸盐恐慌”，乔尔给出了极具说服力的反驳。他指出不仅有一种，而是有700多种肠道共生菌（如乳酸杆菌和双歧杆菌）负责降解草酸盐，并深刻揭示了绿叶蔬菜中硝酸盐对于口腔硝酸盐还原菌转化亚硝酸盐、进而保护心血管糖萼的“不可替代性”。这在逻辑上形成了一个完美的闭环：为了避免极低概率的草酸结石而放弃富含硝酸盐的植物，等同于为了躲避流弹而拆除了心血管防御的城墙。不过，他假设94%的现代人肠道菌群都能有效处理草酸盐，可能过于乐观。在抗生素滥用和高度加工食品普及的今天，大众的肠道屏障极度脆弱，对于已有草酸钙结石病史的人群，脱离临床指导直接进行“草酸脱敏”依然存在急性风险。

4. 蜂蜜松属素与天然GLP-1激动剂的剂量局限性 乔尔试图利用食物组合（乳清蛋白、抗性淀粉、脂肪、甜菊糖、蜂蜜的预负荷餐）来模拟GLP-1药物的饱腹感信号，在机制机制上是成立的，这利用了肠道L细胞和K细胞对氨基酸和短链脂肪酸的受体反应。同样，强调蜂蜜中松属素的抗癌、抗炎等多效性药理价值，在体外细胞实验和动物模型中确有文献支撑。但他忽视了“剂量”的药理学铁律。在真实世界的饮食中，通过食用蜂蜜摄入的松属素浓度极低。

主持人 Lucas Owen 在本期《Boost Your Biology》播客中，再次邀请到功能营养学领域的专家 Joel Green，Joel 在功能营养、减脂、免疫系统优化等方向拥有独到且原创的见解，此次对话围绕其个人健康经历、营养理念、肠道菌群与食物作用等内容展开。Joel 首先回顾了自己踏入健康领域的起点，他自身并非拥有优良的遗传背景，母亲一生受低血糖困扰并因癌症离世，父亲则患有糖尿病，最终因糖尿病相关的肾脏问题去世，这样的家庭背景让他从小便重视健康，母亲在他五岁时就向他强调健康的重要性。他早年通过电视上的 Jack LaLanne 节目接触健身，在七十年代四年级时恰逢跑步热潮，开始绕街区慢跑，五年级时又因电视节目开始每日短跑，追求速度提升，同时也在年幼时就关注健美赛事，通过《Wide World of Sports》观看每年的奥林匹亚先生大赛，对 Frank Zane、Arnold Schwarzenegger 等选手印象深刻。他在中学与大学时期是田径运动员，主攻十项全能，长期保持运动习惯，成年后也一直持续学习与实践健康相关知识。

九十年代初，MetRx 补剂问世，Joel 成为其使用者，这款由 Scott Conley 博士研发、Jeff Everson 与 Bill Phillips 推广的产品，在当时颠覆了健身补剂领域，此前的代谢优化剂多是效果不明的糊状产品，仅通过使用类固醇的健美运动员展示效果，而 Joel 使用 MetRx 后，配合训练与短跑，体脂率降到极低水平，也因此被身边人追问减脂秘诀。但在使用该产品四五年后，他出现了无法控制的暴饮暴食问题，这一经历成为他深入研究健康与营养的核心契机，后来他意识到，自己当时打乱了所有调控进食的激素。此后他尝试过纯净生食、宏量营养素计算等多种饮食方式，却都陷入减脂后体脂快速反弹的循环。2003 年，他进入科技行业的初创公司工作，每日工作 14 小时，长期高压、年龄增长与不规律的生活，让有着 30 多年健身经历、当时 42 岁的他体重大幅上升，增重 35 至 40 磅，体型肥胖、耐力与心肺功能大幅下降，尽管仍有肌肉基础，但身体状态极差。一次与邻居家 16 岁孩子摔跤时，他仅一分钟就体力不支，这件事成为他做出彻底改变的转折点，他决心找到能适配高压全职工作的可持续减脂方式。

随后 Joel 打造出当时全美排名第二的减脂网站，仅次于 WebMD，又在 2007 年发布了面向公众的首篇关于肠道菌群与减脂的文章，并研发出基于肠道微生物组的软件。他通过实验找到能重塑肠道菌群的饮食模式，短短七天后，水下称重测量体脂率仅为 6.7%，这一结果曾受到 Mark Bell 的质疑，他也提供了原始数据证明。这款软件后来被企业、医院与城市采购使用，在服务数千名企业员工的过程中，他彻底改变了对肥胖的认知，不再认为肥胖仅仅是缺乏自律，而是发现多数肥胖人群是无法规律运动的职场久坐者，这一群体才是减脂方案的核心服务对象。他通过软件积累了超过 15000 名用户的数据，总结出高效的健康方案，之后还与 Quest Nutrition 有过短暂的咨询合作，结识了该品牌创始人 Ron Penna，并将自己十年研究的方案整理成书，其中以肠道方案最为火爆，该方案通过针对性喂养特定细菌，恢复人体年轻时的免疫状态，核心是作用于嗜黏蛋白阿克曼菌与拟杆菌门，依靠这两类菌群的相互作用实现免疫系统重置。

主持人 Lucas 提到自己重新重视短跑，认为短跑是减脂最高效的运动，并向 Joel 询问其短跑经历与当前的运动习惯。Joel 表示短跑从青少年时期就伴随自己，他高中是优秀的田径运动员，大学也参与过一年田径赛事，二十多岁时仍会常去跑道跑 200 米，三十多岁也坚持该习惯，46 岁生日时还完成了自制的 “Man Tathlon” 挑战：手提两个总重 90 磅的 5 加仑水壶，攀爬垂直高度 1000 英尺的山坡一英里后返程，紧接着全力冲刺 200 米，且成绩优异。他在自己的第一本书《The Immunity Code》中提出，能否短跑是衡量生理年龄的真实标准，即便生理检测显示年轻，无法短跑也意味着身体状态衰老，他还在书中提出无需热身的短跑理念，这一观点后来被广泛传播。如今随着年龄增长，他偶尔会因受伤暂停训练，恢复时需要数周重新积累状态，但短跑始终是他不会放弃的运动，他认为短跑是提升激素水平、改善情绪、降低体脂最有效的方式，也是对身体挑战最大的训练，例如全力完成 6 组每组 30 秒以内的 200 米冲刺，是极具强度的训练。

Joel 在新作《The Way, The Immunity Code Diet》中，试图厘清各类被饮食派系批判的食物争议，包括草酸盐、燕麦、蜂蜜、植酸等，他会针对同一食物分别阐述支持与反对的核心论点，打破非黑即白的认知。其中蜂蜜常被批判为只是单纯的糖，而深入研究后他发现，蜂蜜的成分极为复杂，因蜜种不同差异巨大，其中含有海藻糖等特殊糖类，还有多种独特的黄酮类物质，其中一种黄酮类物质更是成为药物研发的靶点，现有研究显示其具备抗癌、改善抑郁、缓解炎症等多种积极作用，药企正围绕这一单种黄酮类物质研发三四十种药物。Joel 借此指出，当下营养学存在过度简化的问题，人们将食物简单归为碳水、宏量营养素等标签，陷入语义层面的认知局限，忽略了食物中复杂活性物质的价值。主持人也提到，Joel 是第一个向他介绍海藻糖的人，这种功能性糖类有着多样的应用价值。

主持人进一步询问 Joel 对菜籽油、红花籽油、葵花籽油等植物油与饱和脂肪对立观点的看法，Joel 提出核心前提：食物对人体的作用并非一成不变，当下营养学普遍忽视时间变量，而人体存在累积、降解、代偿、衰减四种内在机制，会随时间改变食物的作用效果，因此必须脱离 “好与坏” 的绝对化范式。以饱和脂肪为例，人们要么认为饱和脂肪被研究证伪、可大量摄入，要么认为其确凿有害，而实际情况是，同一饱和脂肪在不同年龄阶段作用截然不同，20 至 30 岁时，大量摄入鸡蛋、黄油、肉类等饱和脂肪食物，身体可良好适应，但 50 岁后，血管状态发生改变，相同的饱和脂肪摄入可能引发病理性问题。

从研究数据来看，即便被广泛批判的菜籽油，也有研究显示其在血管健康、甘油三酯、血脂相关指标上存在积极作用，其机制与血管内皮的 NOX 酶（NADPH 氧化酶）密切相关，NOX 酶是人体唯一产生自由基的酶，分布于血管内皮，核心作用是调控自由基生成、维持葡萄糖稳态与一氧化氮介导的血管舒张，年轻时该酶功能正常，通过产生过氧化氢调控葡萄糖转运路径，而随着年龄增长，NOX 酶功能失衡，过度产生自由基，导致葡萄糖转运受损，同时大幅改变身体对饱和脂肪的处理方式，使其从无害变为有害。这一过程还伴随糖萼激素的下降，糖萼是血管内的张力感知结构，如同汽车减震器，衰老后糖萼流失、NOX 酶过度激活，会共同引发血管功能异常，诱发心血管疾病。因此饱和脂肪并非绝对好坏，而是由年龄、血管内皮状态、NOX 酶激活状态共同决定。

Joel 还指出，当下营养领域的派系对立，都忽略了时间与身体状态的核心变量，他在书中能为任何对立的营养观点都做出有力论证，但这并非传递真相。真正的核心是，被对立派系批判的食物往往存在协同作用，肉食与植物并非相互排斥，植物能中和肉食中的潜在毒性，肉食则弥补植物的营养缺陷，二者协同保护健康，而非单纯对立。

谈及肉类中的活性肽，Joel 表示这类物质的健康价值常被忽视，其中一类关键肽段作用于血管紧张素转换酶与肾素 - 血管紧张素系统，对血压管理、体液平衡调控具有强效作用，新冠疫情后人们意识到，ACE 受体与代谢健康密切相关，而肉类中的肽段对该系统的正常运作至关重要，此外肉类还含有 BPC-157 等多种活性肽。他强调，肉类是上消化道的最优食物，而植物则是下消化道的最优食物，二者高度协同。

肠道共生菌群与免疫系统深度绑定，双歧杆菌参与肠道抗原感知与树突状细胞的抗原摄取，嗜黏蛋白阿克曼菌则调控 T 细胞比例，二者协同作用，是免疫系统正常运作的核心。极端的纯荤食饮食会导致每日 10 至 15 克氨基酸进入结肠，发酵这些氨基酸的细菌均为促癌菌，例如具核梭杆菌，而植物与肉食均衡摄入时，肠道发酵位点会从蛋白质发酵转向碳水发酵，菌群结构趋于平衡，中和肉食的潜在负面影响，同时保留其营养价值。

对于草酸盐含量较高的羽衣甘蓝、菠菜等蔬菜，当下主流观点多主张避免食用，Joel 则指出这一认知存在巨大漏洞，传统观点认为草酸盐有害且应彻底规避，但现有研究证实，肠道中有超过 761 种细菌可降解草酸盐，包括乳酸杆菌、双歧杆菌等共生菌，过去认为仅草酸杆菌能解毒草酸盐的结论早已被推翻，实际是菌群网络共同完成解毒。自然环境中的生存模式也印证这一点，人类在野外觅食时，会自然摄入含草酸盐的植物，而这类食物恰恰能刺激草酸盐降解菌的生长。

草酸盐是否产生危害，取决于肠道菌群的肠型与组成，当肠道菌群优化，乳酸杆菌、双歧杆菌、阿克曼菌等共生菌丰度充足时，人体可在正常范围内解毒草酸盐，同时获取蔬菜中的营养。而其中关键的前提是，口腔中必须存在硝酸盐还原菌，这类菌群由饮食中的硝酸盐喂养，而高草酸盐的绿叶蔬菜正是硝酸盐的重要来源，随着年龄增长，硝酸盐转化为亚硝酸盐的过程是维护心血管健康的核心，能改善糖萼流失与 NOX 酶过度激活的问题，被主张规避的高草酸盐蔬菜，恰恰是解决心血管衰老问题的关键。克利夫兰诊所、哈佛大学的专家也在研究中证实，应通过优化肠道菌群解毒草酸盐，而非彻底规避。

Joel 强调，这一结论同样适用于正态分布人群，94% 的普通人群在优化菌群后，可适量摄入高草酸盐蔬菜并获益，仅少数存在特定病理问题的人群需要规避，任何营养建议都不能脱离人群差异绝对化。他也主动提出，愿与 Paul Saladino、Sean Baker 等主张彻底规避草酸盐的学者公开辩论该议题。

Joel 再次强调嗜黏蛋白阿克曼菌的重要性，该菌于 2004 年被发现，他在 2007 年便开始重点研究，是肠道黏液层健康的核心菌群。阿克曼菌以肠道黏液中的黏蛋白为食物，会适度变薄黏液层，但其代谢产物会激活黏液层相关基因，最终生成更厚、更具屏障功能的黏液层，同时调控免疫系统，影响 T 细胞、IgA 与抗原感知，与双歧杆菌协同作用，优化肠道免疫环境。

该菌的独特之处在于，其偏好内源性氮源（肠道自身分泌的黏液），饮食中外源性氮过量反而会降低其丰度，它主要定殖于肠道黏膜而非肠腔。阿克曼菌的生长受浆果中的酚类物质与乏食的促进，乏食状态下内源性氮分泌增加，可一定程度补充阿克曼菌，但过度乏食会导致该菌过量增殖，过度消耗黏液层，引发肠道屏障损伤，如同饥饿状态下肠道黏膜会被严重破坏，因此其丰度需要平衡。此外，阿克曼菌参与血糖调控，是天然的 GLP-1 激动剂，能在肠道内触发 GLP-1 分泌，改善胰岛素敏感性。

当下司美格鲁肽等 GLP-1 激动剂药物成为减脂热点，Joel 表示，药物是人工合成的 GLP-1，半衰期更长、效果更强，食物无法完全替代，但通过食物组合与进食时机，可有效激活内源性 GLP-1 与 GIP。他早在 2012 年推广自己的营养软件时，就已将肠促胰素靶点作为核心原理，当时该理念尚不被主流医学界熟知，如今已成为大众关注的焦点。GLP-1 与 GIP 协同又相互拮抗，分别调控脂肪燃烧与储存，糖尿病患者中 GIP 的作用更为关键，这也是替尔泊肽效果优于单一靶点药物的原因。

日常食物中，鸡蛋、蛋白质与可发酵纤维的组合能强效激活 GLP-1，例如牛排搭配土豆，蛋白质与发酵性碳水的协同作用，远强于单一食物。蜂蜜与甜叶菊也具有协同激活效果，他在新书中设计了 GLP-1 奶昔，将乳清蛋白、蜂蜜、甜叶菊、坚果酱与抗性淀粉组合，多重刺激 GLP-1 分泌。而比食物组合更关键的是进食时机，这类组合食物在正餐前 20 分钟摄入，即餐前预载，能最大化激活肠促胰素，乳清蛋白改善胰岛素敏感性、抗性淀粉提升脂肪氧化、脂肪与天然甜味剂协同刺激 GLP-1，形成食物层面最高效的肠促胰素激活方案，虽效果不及药物，但易于日常实施，能有效提升饱腹感。

Joel 还补充，食物进食顺序同样重要，优先摄入蛋白质能提前激活饱腹信号，而多数人仅食用牛排时无法获得充足饱腹感，搭配碳水化合物后，才能产生满足感，这也与肠促胰素通路密切相关。他认为，未来 5 至 10 年，肠道菌群与肠促胰素相关的营养研究，将成为健康领域的核心方向。

对话最后，Joel 表示自己从 2006 年至今，所有研究都围绕一个核心：在真实高压的生活场景下，实现体重与衰老的可控，解决职场人群无法规律运动、时间有限的健康难题。如今他已完成核心方案的研发，新作也已发布，未来将重点推广自己的健康理念，通过播客、社交平台传递内容。他的个人官网为veepnutrition.com与 theic.health，社交账号包括 Instagram、X、TikTok，均为 real Joel Green，新作也将在亚马逊上架，其肠道调理方案也新增了 NAC、甘氨酸等成分进行优化升级。主持人 Lucas 对 Joel 的开放、非教条的科研态度给予高度评价，并期待未来双方的第三次对话。

【观点分析】

1. Joe的整体框架跳出了当下营养领域的派系对立，以时间变量、身体状态、肠道菌群、个体差异四大核心，替代非黑即白的 “好 / 坏食物” 思维，这一点与主流循证营养学的个体化趋势高度契合。其强调的肠道菌群解毒、食物协同、肠促胰素时序激活、生理年龄以运动能力为标准等观点，具备扎实的基础研究支撑，尤其对草酸盐、饱和脂肪、蜂蜜等争议食物的解读，有效纠正了极端饮食派系的简化谬误，对普通大众具有极强的实践指导意义。

   
   肠道菌群对草酸盐的代谢、NOX 酶与血管衰老的关系、阿克曼菌的生理功能、GLP-1 的食物调控等内容，均符合胃肠病学、代谢科学与心血管研究的主流共识。

   反对极端荤食、极端素食、极端避草酸盐、极端避脂肪等立场，与权威机构（WHO、美国心脏协会、内分泌学会）的膳食建议一致。

   强调 “无运动能力人群是减脂核心群体”，贴合公共卫生对职场久坐人群的干预方向。

   
   

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卢卡斯・欧文欢迎乔尔・格林再次做客播客，介绍乔尔在功能性营养、减脂、免疫系统优化等方面是 “行家”，并表示自己很敬佩乔尔，因为他分享的信息极具原创性。

乔尔・格林分享了自己的健康优化之旅。他表示，自己的健康基础并不理想，母亲一生受低血糖困扰，最终死于癌症；父亲是糖尿病患者，因糖尿病相关的肾脏问题去世。因此，健康从小就对他至关重要，母亲也从他很小的时候就强调健康的重要性。大约 5 岁时，他通过电视上的杰克・拉兰内接触到健身，从此健身就融入了他的生活。 70 年代跑步热潮兴起时，他正在四年级，觉得跑步很酷，就开始绕着街区跑步。后来在五年级开始短跑，每天都练，想跑得更快，因为当时 50 码短跑是件很流行的事。他小时候还很喜欢健美，会看《体育大世界》节目，里面每年会播放奥林匹亚先生大赛，他记得弗兰克・赞恩获胜，以及阿诺德和他的互动。 他在高中和大学都是田径运动员，参加十项全能比赛，短跑成为他一生坚持的事情，即使在二十多岁时，也会去田径场跑 200 米。46 岁生日时，他还进行了一项名为 “男子十项全能” 的活动：提着两个 5 加仑的水壶（重 90 磅），在 1000 英尺垂直高度的山坡上往返一英里，然后全力跑 200 米，而且成绩还不错。 他坦言自己本质上就是一个 “消费者”，一生都在不断吸收健康相关的知识。90 年代初，MetRx（美瑞克斯）问世，他开始使用该产品。他提到，在 MetRx 出现之前，市场上有一些所谓的 “代谢优化剂”，其实就是一些糊状的东西，装在小袋子里，商家会告诉消费者这东西有效果，还会找一些使用类固醇的健美运动员做宣传，声称是产品的功效。而 MetRx 由斯科特・康利博士推出，杰夫・埃弗森和比尔・菲利普斯对其进行了大力推广，其最初的产品效果显著。 大约四五年后，他开始出现无法控制的暴饮暴食情况，这成了他在健康和健身领域探索的一个重要转折点。他当时不知道原因，后来才明白是自己调节食物摄入的激素失调了。这之后的一段时间里，他不断尝试不同的饮食方式，2000 年左右，他尝试过全生食、新鲜食物，也试过计算宏量营养素，精确到克，但结果总是相似：先是变得很瘦，然后又重新发胖。 2003 年，他进入一家科技公司工作。那段时间，很多现在很有名的人也在同一个行业，他们彼此是客户，互相认识，有些名字可能会让人惊讶。这段经历对他影响很大，因为他在进入公司前，刚刚完成了一次营养方面的尝试，当时身材很好，有腹肌；但在公司工作期间，由于是初创公司，业务增长很快，他每天工作 14 小时，压力极大，每天都有各种问题需要解决。到 2006 年左右，年龄和压力的影响显现出来，他离开公司时，体重增加了 35 到 40 磅，达到 260 磅，虽然肌肉量很大（因为一直在锻炼），穿 3X 的衬衫，现在穿 1X，但身材肥胖，没有耐力，也无法做有氧运动。 一个重要的改变发生在他和邻居家的孩子摔跤时。一个 16 岁的孩子想和他摔跤，他只坚持了大约一分钟就气喘吁吁，这让他决定做出彻底的改变，重新变得 lean，并想办法在全职工作的重压下保持这种状态。这一决定改变了一切。后来，他创建了网络上排名第二的减肥网站，仅次于 WebMD，还开发了一款基于肠道菌群的软件。2007 年，他撰写并发表了第一篇面向公众的关于肠道菌群与减肥的文章，至今仍可查阅。 他进行了一些实验，最终发现了一些饮食模式，主要是通过喂养特定的细菌，来重建年轻时的免疫系统，这基于 Akkermansia muciniphila 和参与免疫的 phytobacteria 家族之间的相互作用。如果能喂养这些细菌，实际上可以重置年轻时的免疫系统，效果显著。通过这款软件，他能看到不同人的结果以及他们所采用的方案，因为软件中包含很多变量，会根据用户的情况（比如有炎症就从饮食中去除西红柿）提供不同的食物方案，这帮助他总结出有效的方案。 到 2013 年，已有超过 15000 人使用过这款软件。卢卡斯询问这款追踪软件是否类似 chronometer 或热量计算工具，乔尔表示并非如此，它是通过视觉识别盘子里的食物来实现的，不涉及热量计算，但他能从后台看到相关结果，从而总结方案。不过，他当时不太了解企业健康管理，期间有成功也有失败，但这段经历让他明白了很多有效的方法。 之后，他与 Quest Nutrition 有过短暂的咨询合作，在那里认识了很多优秀、聪明的人，包括 Quest 的创始人罗恩・彭纳。有一天在一次圆桌会议上，每个人都有自己的见解，他也有自己的想法，他觉得需要写一本书来解释这些内容，于是他的第一本书就应运而生。书中收录了他过去大约 10 年总结出的所有方案，其中 “肠道方案” 尤其受欢迎，大致内容是通过喂养特定细菌来重建年轻时的免疫系统，这一方案大获成功，也让他一路走到了今天。

卢卡斯提到自己现在更多地开始进行短跑训练，觉得短跑是减少体脂最有效的运动，询问乔尔当年的短跑训练情况，以及他现在是否还进行短跑，训练方式有何变化。

乔尔表示，短跑从他十几岁起就成为生活的一部分。他在高中时是不错的田径运动员，大学也跑了一年，还参加过十项全能比赛。整个生活中，短跑都是他会做的事，二十多岁时，他会去田径场跑 200 米。他甚至有自己三十多岁时去田径场跑 100 米的视频。46 岁生日时，他还进行了一项名为 “男子十项全能” 的活动：提着两个 5 加仑的水壶（重 90 磅），在 1000 英尺垂直高度的山坡上往返一英里，然后全力跑 200 米，而且成绩还不错。 他在自己的第一本书《免疫力密码》中提出，真正的年龄测试是能否短跑。生物测试可能会显示 “年轻 10 岁”，但如果不能短跑，就不算真正年轻。年轻人能随时短跑，甚至不需要热身，他在书中提到的 “无热身短跑” 后来被广泛传播。 现在，随着年龄增长，他偶尔会受伤，需要休息几周，之后又得重新开始，需要几周时间才能恢复到之前的状态，但他可能永远不会放弃短跑。他认为短跑能有效提升激素水平、改善情绪、减少体脂，是对身体最具挑战性的运动之一，比如在田径场上跑 6 个 200 米，每个都努力跑进 30 秒以内，这是非常高强度的训练。

卢卡斯提到乔尔最近发布的内容中谈到蜂蜜中一种天然存在的黄酮类化合物松属素（pinose sembran，推测为 pinostrobin），询问是什么引起了乔尔对这种黄酮类化合物的兴趣。

乔尔表示，他的新书《The Way, The Immunity Code Diet》旨在消除人们对不同食物话题的困惑，其中探讨了草酸、燕麦、蜂蜜、植酸等被某些饮食群体诋毁的食物，并对这些食物进行了详尽的分析，甚至在书中有一个章节从正反两方面进行论证，比如分别列出支持吃肉和反对吃肉的最佳论据，以此展示从不同角度都能进行有说服力的论证。 在研究蜂蜜时，他发现蜂蜜是一种独特的存在，其成分因品种不同而有很大差异，含有多种特殊的糖类（如海藻糖等）和黄酮类化合物，而松属素就是其中一种。研究表明，这种黄酮类化合物在药物研发领域有广泛应用，似乎对人体生物学的几乎每个领域都有积极影响，如抗癌、改善抑郁症、缓解炎症等，有 30 到 40 种不同的药物研发都与这种单一的蜂蜜黄酮类化合物有关。这也说明，那种将食物简单归结为宏量营养素（如认为蜂蜜只是碳水）的简化观点，可能会让人们忽略很多重要的东西，而人们在这个时代容易被用词所 “语义操控”，从而错过事物的本质。 卢卡斯表示自己对食物中发现的一些黄酮类化合物很感兴趣，松属素就是其中之一，还提到乔尔是第一个向他介绍海藻糖的人，这是一种用途广泛的功能性糖类，询问乔尔是否仍在使用，是否有新的应用。随后，卢卡斯将话题转向植物油（如菜籽油、红花油、葵花籽油）与饱和脂肪的争论，询问乔尔是否从正反两方面对此进行过研究。 乔尔认为这是一个有趣的话题，首先需要明确一些基本规则：同一种食物在不同时期对人的影响可能完全不同，不能认为某种食物永远好或永远坏。这是因为人体内存在积累、降解、补偿、衰减四种力量，它们会随着时间改变食物对人体的作用。以饱和脂肪为例，人在 20、30 岁时，可能可以大量食用鸡蛋、黄油和肉类而无不良影响，但到了 50 岁左右，随着血管状态的变化，同样的饱和脂肪可能会产生病理影响，所以这不是非黑即白的问题，所有食物都是如此。 谈到不同种类的油，从研究来看，即使是被诋毁的油，也能找到很多益处。以菜籽油为例，虽然他个人不喜欢菜籽油，但纯粹从实证角度看，有研究显示菜籽油有诸多好处。 乔尔进一步解释，血管中有一种叫做 NOX 酶（NADPH 氧化酶）的物质，这是人体已知的唯一能产生自由基的酶，它们分布在内皮细胞和血管中，有多种功能，其中最重要的是在特定时间和方式下调节自由基的产生，以维持葡萄糖稳态、一氧化氮生成和血管介导的血管舒张。年轻时，这些酶能正常工作，产生的过氧化氢会与磷酸酶相互作用，从而有助于葡萄糖转运。但随着年龄增长，这些酶会失调，过度产生自由基（过多的过氧化氢），这会损害葡萄糖转运，更重要的是，会极大地改变人体处理饱和脂肪的方式，一旦 NOX 酶功能失调，原本可能无影响的饱和脂肪就会变得非常有害，这种情况通常与糖萼激素的下降同时发生。 糖萼是血管内的一种类似 “毛发” 的张力传感器，能根据血流和血管舒张感知张力，就像汽车的减震器一样重要。随着年龄增长，NOX 酶过度产生自由基，干扰血管内皮中一氧化氮的正常生成，同时糖萼减少，血管状态改变，从而增加心血管疾病的风险。因此，饱和脂肪的影响并非绝对的好或坏，而是取决于人的年龄以及血管、内皮和 NOX 酶的状态。 在看待不同种类的油时，即使是那些被诋毁的油，也能在研究中找到其益处。比如菜籽油，有研究显示它在血脂、血管健康、胆固醇相关问题等方面有帮助，他虽然不喜欢菜籽油，但如果要为其辩护，可以引用这些研究；反之，也可以从草甘膦等角度提出反对意见。但人们往往忽略了时间的影响，时间会改变一切。 对于天然食物而言，那些被对立的食物群体其实是相互作用、协同增效的。比如，喜欢吃肉的人所诋毁的植物，其实能保护人体免受肉类中的毒素影响；反过来，肉类也能弥补植物的不足。这种协同作用在共生细菌方面体现得尤为明显，因为共生细菌与免疫系统密切相关。例如，双歧杆菌家族与抗原感知密切相关，能促进抗原被树突细胞吸收；肠道内的 Akkermansia 与 T 细胞调节等有关，它们之间协同作用，没有这些细菌，就很难实现真正持久的健康。 当饮食中同时包含植物和动物食物时，发酵的场所会从蛋白质发酵菌转向糖分解菌（碳水化合物发酵菌），从而达到平衡，避免负面影响，同时获得肉类带来的益处，两者协同作用显著。

卢卡斯提到乔尔对肉类中现已发现的肽也很感兴趣，这些肽可能带来我们从未考虑过的重大健康益处，询问到目前为止，在这些肉类中的肽对健康的影响或对代谢功能的作用方面有哪些发现。

乔尔表示，肉类中的肽在血管紧张素转换酶和肾素 - 血管紧张素系统（与血压调节相关）方面的作用可能未被充分关注。肉类中含有非常有效的抗高血压肽（如 APPV4 等），不仅对血压有积极影响，还对肾素 - 血管紧张素系统的调节有好处。过去认为该系统仅与体液平衡有关，但在新冠疫情后，随着对 ACE 受体的关注，人们发现代谢健康在很大程度上也依赖于 ACE 受体及相关物质的正常运作，而肉类中的这些肽对此有很大益处。 此外，肉类中还有多种其他肽，比如众所周知的 BPC 157 等。肉类对人体至关重要，尤其对 upper gut 来说，是最佳食物；而植物是 lower gut 的最佳食物，两者协同作用显著。 卢卡斯分享自己多年来对所吃蔬菜很挑剔，现在主要吃胡萝卜、洋葱、白蘑菇，尽量避免羽衣甘蓝、菠菜等高草酸蔬菜，询问乔尔对人们对这些蔬菜的耐受度有何看法。 乔尔指出，人们对草酸的认识存在一个很大的漏洞，即普遍认为含草酸的食物不好，应该避免，但忽略了一个事实：肠道中有超过 761 种细菌能分解草酸，这些细菌大多是共生菌，如乳杆菌、双歧杆菌等，而以前认为只有 O-forma genes 能分解草酸，事实并非如此，而是一系列细菌共同作用。 自然界中存在一种可验证且可重复的饮食模式：当人处于自然环境中，会立即开始觅食，所吃的食物中可能包含含草酸的绿叶蔬菜等，而自然界的设置是，这些食物会刺激肠道中分解草酸的细菌。 随着年龄增长，保持心血管系统的最佳状态至关重要，而这需要口腔中存在硝酸盐还原菌，这些细菌依赖饮食中的硝酸盐（如绿叶蔬菜等含草酸的食物中的硝酸盐）。如果饮食中缺乏这些，随着年龄增长，硝酸盐向亚硝酸盐的转化就会受影响。而含硝酸盐的蔬菜等正是解决 NOX 酶过度激活、糖萼减少等问题的关键，这些被认为应避免的食物实际上能解决人体面临的重大健康问题。 克利夫兰诊所、哈佛的亚伦・米勒等专家也认为，应更重视通过饮食（即培养能分解草酸的肠道菌群）来分解草酸。但需要注意的是，一切都呈钟形曲线分布，中间 94% 的人在优化肠道菌群后，适量食用含草酸的食物可能不会有太多问题，还能获得益处；而处于曲线两端的少数人，尤其是有健康问题的人，则可能不适用。不能用非此即彼的思维来看待这个问题。

卢卡斯提到自己和乔尔都了解阿克曼氏菌（Acomansia，推测为 Akkermansia）的重要性，让乔尔提醒听众这种细菌的重要性。

乔尔介绍，阿克曼氏菌于 2004 年被发现，他在 2007 年开始关注它，另外还有 Fecalibacterium prausnitzii 也很重要，但阿克曼氏菌是主要的。它是负责肠道粘液层健康的主要细菌，以肠道粘液层中的粘蛋白（糖蛋白）为食，在分解这些物质的过程中，会产生代谢物并激活肠道粘液层中的基因，从而促进更厚、更坚固的粘液层形成，这通常是有益的。 阿克曼氏菌与免疫反应密切相关，能调节人体免疫系统的多个途径，如调节 T 细胞、免疫球蛋白 A（IgA）、抗原感知等，与双歧杆菌协同作用，通过选择性喂养这两种细菌，可优化肠道内的免疫环境。 阿克曼氏菌更喜欢内源性氮（即粘液分泌物）作为食物来源，饮食中的外源性氮可能会减少其数量，它主要生活在肠道内壁而非肠腔中，当肠腔中氮过多时，可能会在一定程度上抑制阿克曼氏菌。 阿克曼氏菌的生长得益于浆果中的酚类物质和乏食，因为乏食时能为其提供内源性氮。但它也是一把双刃剑，过度乏食或某种因素导致其过多，可能会磨损肠道内壁，就像在饥饿状态下，肠道内壁会被严重磨损一样，因此需要平衡。 此外，阿克曼氏菌还与血糖控制有关，

继续

能帮助胰岛素有效发挥作用，它还是一种 GLP-1 激动剂，当体内存在阿克曼氏菌时，能刺激肠道产生 GLP-1。总之，了解这种细菌并知道如何喂养它，能带来很多益处，这也是《免疫力密码》一书传达的要点之一。

卢卡斯提到 GLP-1 激动剂是当下的热门话题，如司美格鲁肽等化合物，不仅能通过抑制食欲帮助减肥，还能作用于许多其他通路，询问乔尔多年来是否发现一些独特的天然 GLP-1 激动剂或刺激 GLP-1 产生的方式。

乔尔表示，合成的 GLP-1 激动剂半衰期与食物不同，效果更强，但了解如何通过食物激活 GLP-1 很有价值。2012 年，他为医院提供营养软件服务时，就涉及到 GLP-1 和肠促胰岛素，当时很多医生对这些概念并不了解，而现在已成为主流。 多种食物都能激活 GLP-1 和 GIP（葡萄糖依赖性促胰岛素多肽），它们既协同作用又相互拮抗，一种能开启脂肪燃烧，另一种可能关闭。在糖尿病患者中，GIP 对血糖控制的影响更大，这也是曼吉妥（Mounjaro）比其他药物效果更好的原因之一。 他常用的天然激活 GLP-1 的食物包括鸡蛋，以及蛋白质与肠道发酵纤维的组合，这种组合能产生协同效应。例如，牛排配土豆，因为肠道中的发酵物质会激活 GLP-1，蛋白质也能激活 GLP-1，两者结合效果很好。蜂蜜和甜叶菊的组合也有协同作用，在他的新书中，有一款 GLP-1 奶昔，将蜂蜜、乳清蛋白、甜叶菊等结合，都能靶向 GLP-1。 时间安排也很重要，食物的食用顺序影响很大。比如，乳清蛋白对胰岛素功能有多种益处，能激活 GLP-1，搭配坚果酱（其中的脂肪也能激活 GLP-1）、甜叶菊和蜂蜜等，效果更佳。再加入抗性淀粉，乳清蛋白与抗性淀粉的组合已被证明能增加脂肪氧化并激活 GLP-1。将这样的组合作为餐前 20 分钟的预加载餐，能产生很强的 GIP 和 GLP-1 激活效果，虽然不如药物强效，但通过食物也能达到不错的效果。

卢卡斯表示未来 5 到 10 年，关于肠道细菌与饱腹感信号等领域的研究将会很有趣，随后询问乔尔的未来计划。

乔尔说，自 2006 年以来，他一直在努力解决一个问题：如何在现实生活中控制身体状态。对于每天工作 14 小时、没时间锻炼的人来说，如何避免发胖和快速衰老，这是他过去 16、17 年的研究重点。现在，他主要致力于传播这些知识，刚完成一本新书，正在参加各种播客活动，希望推广自己的研究成果，接下来可能会更多地关注业务的营销方面，继续自己正在做的事情。 卢卡斯认为乔尔在营养学领域有深刻且独特的见解，且思想开放，不固执己见，值得尊重

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D:2026.04.14<markdown>

00:00

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02:31

Hey everyone and welcome to the Boost Your Biology podcast. My name is Lucas and I am the founder of Ergogenic Health. Together in this podcast series, we will go underground to explore cutting edge health and human performance insights that you simply cannot search on Google to help you upgrade your existence. So without any further ado, let's jump into today's episode.

03:03

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03:24

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03:38

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04:01

Hello, everyone, and welcome to yet another episode of the Boost Your Biology podcast. Today, I'm joined in with a very special guest joining me in all the way from the US. Today, we have Joel Green joining me in to talk all things biohacking, intermittent fasting, a little bit on fat loss, and some other very novel concepts. So Joel, welcome to the show, man. Thanks, Lucas. It's good to be here. Thank you for having me.

04:31

Awesome. So maybe you want to give my audience a bit of a background into, I guess, your story and your mission. Yeah. So I'm very old. I'm 56. So I've been doing this a long time. And I've had… I had the…

04:53

probably a good 30 years doing, doing the fitness thing, you know, that, uh, we've all done it. You know, you just, you're in your teens and twenties and you want to look good and you know, you, you watch pumping iron and you know, you did that thing. So I did that for like 30 years. Um, and, uh,

05:11

going into the 90s, the early 90s, when the modern era of nutrition really began. A lot of people don't know this, but MCTs were introduced in the early 90s and a lot of other things, keto diets and stuff like that. So I was an early adopter for those things. And I read an article by Jeff Everson in 1992 about

05:38

about where he said that he was just eating one meal a day in the evening. And I'd already known that like Herschel Walker, this like a guy who was this amazing athlete, like back in the 80s was doing that. And I was like, wow. So I started doing that and just taking Metrax.

05:58

And this was like probably '92 and it was like in two cans. And I was peeled. I was probably four or 5% body fat. I was ripped. And I had everybody asking what I was doing and, “Tell us your secret.” And what happened to me is what actually nowadays I get a lot of people coming to me, which is after several years of doing that, you basically break your metabolism.

06:25

You know, your hunger is out of control. Your insulin sensitivity is wrecked and all these different things that you'll do if you go down that path. So that happened to me in the 90s. And it was a wake up call for me. And I didn't know what I had done.

06:42

I knew that I did something, but I didn't know what it was. And so the gut hormones at that time hadn't even been discovered and they were just sort of in the research phase. And so I really kind of started what you might call a biohacking. There wasn't a word for it. I was just trying to figure out and experiment with different things. So that led me down a road or probably…

07:07

through 2006 of just trying one protocol after another, trying things like what you would call time-restricted feeding or just clean eating, fresh whole raw, everything fresh whole raw, that phase. And then I had my clean macro phase. I had all these different phases. And what was notable about this thing, two things. Number one,

07:30

I was a regular person. I wasn't getting paid to be fit. So that was number one. And then number two, what was sort of interesting about that was that I was in the real world, I was getting older. Okay, so I was I had passed out of being kind of carefree and single, moved into like my early 40s by 2005. I think I turned 40.

07:55

And so I was just sort of seeing the cumulative effects of all these different things that I'd been doing over the years. And notably what, what I really noticed was that, um, it all broke down, um, under pressure in real life. Like, like it, like,

08:08

And I realized what I was trying to do, same thing everybody else is doing. You're trying to import into a very distinct ecosystem, a bunch of strategies that weren't born in that ecosystem. You're trying to import into the ecosystem of real life where time constraints essentially dictate what you can do with your time, strategies that are born out of an ecosystem where everybody's paid to be fit. And they broke down. It all broke down. So I was…

08:37

I was in a startup company. We became pretty successful. The company, we went from like zero to $2 million a month here pretty fast. And I was working, just working, working, working 14 hours a day. And I had come into that job in probably 5% body fat. I was really in shape. And I left it being 257 pounds. You know, kind of like that, really fat.

09:05

but big, big, big, but fat, you know, like a big arms, big chest, big gut, you know, the whole story. So, uh, coming out of that, uh, it was a big change for me. And I, I, uh, I kind of ran into the problem everybody's going to run into, you know, which is, um, uh, time kind of makes a prison out of the body. And it really kind of formed the core of what I'm doing today. Kind of what I would say my mission is. And that is, um, uh,

09:31

Really, everybody has the same problem with the body. We all face the same problem. It's a problem that time will make a prison out of the body. Time makes a prison out of the body. And it's a prison made from where the bars are invisible, but you feel them. It's declining energy. It's restricted mobility. It's…

09:50

increasing body fat and it's a risk of disease, like cancer and things like that. So that's what time does to the body. And the solution really is to keep the body young. It's just, that's the solution. And what I really have come to realize is that, and this is the premise of my book, “The Immunity Code.” The premise of the book is that real health is missing.

10:17

that we have this endeavor everybody's chasing after. We call it being fit or different words we use on it like weight loss or biohacking. It's all the same sort of thing. And if you look at it and you look at kind of just get out of the selfie, the before after selfie and just kind of track long term what happens, you get a completely different picture of what's really happening. What's really happening is that

10:45

you're over time, you just see that by following most of these strategies, trying to import these strategies out of that ecosystem into the real life ecosystem, what's happening is that, um, it just doesn't work for most people over time. And when you look at their bodies, they're doing this with weight over time. But more importantly, like a lot of the people that you think know what they're talking about are just as cast cancer prone, if not more, uh, just rate of heart attacks is just as, just as frequent, if not more. And so, um,

11:13

When you study it, you see very clearly real health is missing. And there's a long, long list of names of people that I can think of from the past 30 plus years, 40 plus years that are dead, that were once really famous and really fit and famous for being fit.

11:27

And they're all dead, all of them. So they're not living longer. They're not any less cancer prone. So real health is not there. And when you start to peel back, well, why is real health not there? I give the analogy in my book of

11:43

a real guy. I used a pseudonym. I called him Simon. And Simon was a meathead who got on the juice and got super fit. And next thing you know, was running a big supplement business and everybody wanted to know, what's your secret, dude? What's your secret, man? And I knew the secret. The secret was the same secret it's always been. It's a whole bunch of time and a whole bunch of drugs. That was the secret. But I saw a funny thing happen. And

12:11

as the years rolled by, like Simon tried to get off of the juice and he couldn't because when he started getting off the juice, he's like, ah, man, I'm just getting that old man body, you know? And he didn't have the power to control his body. He couldn't get his body to do what he wanted it to do. And that's the problem everybody faces over time. You can't get your body to do what you want it to do. And you'll hear that story more often than not. And the story you most often hear is,

12:38

Well, I tried this program in my 20s and it worked for a while. And then I did this for a while in my 30s and it worked for a while. But now nothing's working and I can't lose weight. It's the power to control the body and to get it to do what you want it to do. And there's really no solution that has ever been proposed to solve that problem. And that's kind of my thing. That's what I'm working on. Because all the solutions that have been proposed…

13:04

they never they never take into account the real world ecosystem see it's like it's one thing to propose some solution that um you know uh takes a whole bunch of time and a whole bunch of energy and often a whole bunch of drugs it's another thing to do it without time and that's the trick is in the real world you have to there's you have these periods where there's no time there just aren't and you have to make it work when there's no time and that's that's

13:27

It's a whole other layer of difficulty. So that's kind of a long-winded what I'm doing. Yeah, really well put, Joel. There's one concept there that I really would love to expand upon, and that is the idea around performance versus longevity. Like this sort of trade-off that was sort of, you know, the quick results with this, you know, steroids, drugs versus, oh, what's the trade-off for longevity and things like that. Yeah. Yeah. Yeah.

13:57

we can we could do an entire show on just that if you wanted to because it's you know there's a lot to that so the first thing to understand is that um

14:11

We get into things like, we want the benefits of things like fasting, for example. We want the benefits, but what are those benefits? And what are the mechanisms that drive those benefits? What are they? Well, it's the only proven model to ever extend lifespan is starvation or just eating less, caloric restriction. Okay, well, that's a huge benefit, right? Well, what's the mechanism? How's it work? Why does it work? Well, when you break that down,

14:40

It gets down to signal pathways, really. And it gets down to the activation of very specific signal pathways that either trigger the body to run through its allotted cycles of growth or put the brakes on one of the two. And so the inherent cost of pushing growth into the body is that you're using it up faster.

15:04

So, now that's fine as long as it's an individual choice, as long as you know what you're doing and you understand that it's very much like a car. It's very much like, you know, let's say the average engine has 100,000 miles in it and you just want to take your car to the track all the time. Well, that's cool. You can do what you want with it. You got to understand that pushing the car…

15:27

in that way is using the life cycle of the car up a lot faster. And the body works very much the same way when it gets down to looking at the way signal pathways work. And there's very good science on this. And I put it in the book in terms of a, it's called the IIS, Signal Pathways Paradigm of Aging.

15:48

And in a sense, aging is somewhat linear with respect to inputs down the insulin, insulin-like growth factor pathway. And in order to grow, we need that pathway to fire. So from a performance aspect, in terms of putting on muscle or things of that nature,

16:09

That requires growth from the body. And there's a balance between too little growth, just enough and too much. And so it's a very interesting topic to think about versus longevity, which is sort of the inverse pathways, things like the AMPK pathway, the sirtuins and different processes like ubiquination and all that stuff.

16:27

So, these things sort of exist, kind of opposed, but also complementary. They work together, but they're also opposed. And it's a big discussion in a big universe to dive into. Yeah. Well, let's sort of segue into a bit about fasting because I know you talk quite a lot about various types of fasting, things like that.

16:52

Firstly, I want to ask you, what can people do to amplify the benefits of fasting?

17:02

Fast less. That would be the first thing. Fast less, yeah. So the first question that I can tell people is, “Well, why are we fasting? What's your purpose in fasting?” And your purpose is probably, “Well, I want to induce autophagy. I want to do all these things.” Well, almost all those things happen during sleep.

17:25

They just happen much better during sleep because that's why we call it break fast. Sleep is fasting. But sleep is fasting done in a way where it syncs to circadian rhythms and it syncs to signal pathway activation. So optimizing sleep is sort of the first level.

17:45

of amplifying fasting, making sure that your sleep is really tracking in all cylinders. That's kind of the first level of it. But beyond that, what I talk about a lot in my book, maybe kind of the core focus is

18:01

there are things that are complementary to fasting. And when we look at what those things are, there's something very interesting that pops up. It's that

18:18

You see that, just to use an ancestral narrative, which by the way, narratives are helpful. They're not facts. They're just narrative and story. They're helpful. I use them. But we always have to remember when we're using narrative that it's just a narrative. Let's see if it correlates to the data. But a very helpful narrative is to understand that historically speaking, when we were starving, pretty much the last thing on the menu is going to be roots.

18:44

Okay. Like it's, I mean, you'll eat them. You'll, you'll dig up roots and eat them if you have to. It's just not your first pick. Your first pick is, you know, probably like a steak or, you know, something else. That's your first pick. But it turns out that, um,

18:58

the way nature has sort of partitioned the economics of starvation, that there's a benefit to roots in a starved state. And it's that roots in a starved state feed bacteria that mimic the effects and enhance the effects of both exercise and fasting.

19:16

So certain types of bacteria proliferate with certain types of food inputs, and those bacteria are commensal, meaning that they're extremely beneficial to their human hosts. And when you look at like, if you were to just draw out a spreadsheet, and how about a selection of checkboxes and compare exercise to certain bacterial metabolites,

19:40

You'd see one-to-one as they're doing the same thing. One is exercise-produce of lactic acid. Certain bacteria, check. Exercise activates the AMPK pathway. Certain bacteria, check. Exercise induces mitochondrial biogenesis. Certain bacteria, mitochondrial microbiome cross-talk, check. And so what we see is that that's very interesting, that in a starved state, certain roots potentiate certain bacteria, which…

20:07

essentially mimic exercise and amplify fasting. And if you can time that to best of all worlds, to the maximum signal induction, diurnally speaking, in other words, during sleep, what you're doing

20:21

is you're inducing um essentially more cells more signal strength for all the things that that make fasting work so that then coming into a fast you don't have to fast as long you just don't have to fast as long and there's and there's good reasons to not fast as long um we see that um

20:42

It's becoming pretty common now because we're getting into year two, three, four for people who've been doing fasting. A lot of people are having a lot of problems with it. The longer that they do it, they're getting into just uncontrollable eating. And those are things to be expected when you look at how leptin works over the long term. So there's very good reasons to want to economize fasting so that you can do it on a regular basis. And then every now and then you want to do an extended fast, you can do that. But in terms of like…

21:09

you know kind of having this unchecked um sort of uh binge on fasting uh there's there's negatives to that and one of those one of those could be sleep disruption so it's something that um there's some very good reasons to want to get as much bang for the buck out of fasting as you can amazing amazing points just uh just mentioned there one of them um one of them really excited me and that is looking at um how yeah obviously how fasting can manipulate

21:37

certain gut bugs and these gut bugs can elicit some of the same effects that fasting has downstream. So I want to discuss one of the key bacterias that we have quite a lot of research around and that is the Accomansia species of bacteria and specifically Accomansia

21:58

I mean, I personally use metformin twice a week. I have certain criteria for using metformin. It's a bit of a weird setup that I have. It's like if I've had a single night of very bad poor sleep or sleep deprivation, I'll use metformin the next day.

22:16

or a day that I don't train, I'll use metformin. And one of the reasons why I'm excited by metformin is the fact that it can increase the akkermansia growth. So do you want to talk about this particular bacteria and why it's so beneficial? Yeah, well, so in the gut, the gut barrier, the gut junction, you have a layer of mucus

22:46

And that layer of mucus is very thin, and it is the only thing separating you from the outside world. So every day, you bring the outside world into your body, and it stays the outside world. It doesn't become part of you. Okay, some of it.

23:01

And so there's kind of a selection process in order to see who gets in the door, who gets into the body. And so when you look at the actual epithelial barrier, you'll see there's this little layer of mucus that's just essentially protecting you from the outside world. And that's no small thing. I use the example in my book of a…

23:20

a piece of salami and just digging and just cutting, if you just cut a square patch where your flesh was exposed and put some salami on that, you'd have a real problem in about an hour or two, like a very big problem. But if you covered that with a layer of mucus,

23:42

we had some protection there, it would be a different story. So that layer of mucus is what protects us from the outside world. And the way that layer is maintained is by a very select, very few number of bacteria. The principal player in that picture is Ackermansia mucinofa. And Ackermansia mucinofa is what's known as a mucin forager.

24:05

These are bacteria that really like olink glycans. They feed on them and they forage for mucin in the gut. So the net effect of these bacteria is that they are probably the most commensal bacteria known in many respects. In other words, that

24:24

our health is so inextricably linked with acromantia and a couple others, fecal bacteria, prosodensia, and beta-bicron, that our health is so linked to these bacteria that we could probably make a list and say, wow, these are really at the top of the list of the most commensal bacteria. And acromantia does a number of things. One of the things it does, well, first of all,

24:48

It just seems to correlate very well to body composition. What you see in obesity is that people who are obese, they just tend to have less acromantia. And then people who are lean and thin just tend to have optimal levels of acromantia. It's not 100%, but it correlates very, very well.

25:11

And there's some good reasons for that. Acromantia seems to have the ability to contract the surface area of the gut. So actually, actually can help, help us absorb fewer calories, simply contracting the surface area of the gut. Yeah. It's also seems to be involved in cold induction. So cold and acromantia seem to work and seem to work together. And it's,

25:36

Basically, it maintains the integrity of the gut barrier. It's very, very much involved in maintaining a healthy immune system. So the way the immune system typically works is that in the gut junction, in the epithelial barrier, we have dendritic cells that will sample antigens and sample the gut lumen. And acromantia does a number of things to sort of keep that whole

26:01

optimal and keep our immune system working. So it's extremely important. We also see it in autoimmune disease. So curiously enough, I mentioned this in the book, I mentioned the case of MS, but you can see it in other autoimmune disease as well, where you get too much achymanthia and it becomes a problem. And it's probably a case where…

26:24

there is an over polarization of immune signals coming from things like interferon gamma, which is stimulating populations of acromantia. But it's just an extremely fascinating sort of field of study. Yeah. Fascinating. Interesting. So what about, let's sort of segue into, I guess, maybe

26:48

We touched on metformin. I'd like to hear your stance on this particular, you know, medication for, I guess, longevity, performance. Yeah. Things like that. Yeah. You know, I think metformin is one of those wonder drugs. You know, there are a number of drugs out there that are wonder drugs. I mean, we're lucky to have them. And I think metformin is probably one of them. Yeah.

27:15

I don't take it personally, but I will eventually. I'm saving it for the finish. But yeah, I think metformin is best used sort of intermittently and strategically. So it's not something I would use every day. It's not something I would use on a continual basis. But I do think that there's a very good case for seasons of metformin and using it very strategically, like the way you're using it for

27:43

it for example yeah um i think in that case it's a wonder drug i mean you know it it helps us age slower um probably keeps the mitochondria in better shape uh as long as we're kind of not overdoing it and you know just as a number of really fantastic things yeah awesome awesome yeah i tend to with the the metformin usage um yeah again like i said very strategic about when i'll

28:08

you know, deploy it or rotate it with other insulin sensitizing agents. Um, but ultimately like nothing will be, you know, I mean, I, I aim to get 20,000 steps in a day. So there, there was a study where they compared, you know, um, 15 minute brisk walk versus metformin, you know, post, uh, postprandial glucose levels and walking out performed metformin. So I think I'm getting the best of both worlds there. So, um,

28:37

Yeah, I would agree with that. Yeah. That gets to another fascinating topic, which is exercise-induced glucose transport. And what's interesting about that is that it can work locally as well. So, kind of the myth of spot fat reduction and all that. Well, when you look at exercise-induced glucose transport,

28:59

uh you can get sort of insulin resistant pockets in the body particularly in adipose mass and exercise or just muscles contracting uh works as a works as a sort of an insulin pneumatic so

29:13

when you have problem areas and you have things typically in the belly or things like that. What you'll see very often with very specific areas in the belly is you'll see hypoxia and you'll see insulin resistance. And so glucose transport's impaired. And just muscle contractions. When you look at people who are…

29:32

move their muscles, move specific muscles a lot. They're always lean in those muscles. And I believe it's because exercise and muscle contraction is so good at keeping glucose moving, shuttling back and forth and mimicking insulin. Yeah, that's fascinating. That's something worth exploring more of. So Joel, let's sort of segue and discuss a little bit around

29:56

I know there's one video on trending quite well. They're talking about the metabolic fate of alcohol and how we can biohack that. So let's talk about, yeah, let's talk about alcohol and how we can just work around that.

30:10

Yeah, that's a big one. People want to know that. Yeah. Well, first thing, alcohol does not make you fast by itself. It actually helps you get lean, if anything. It's thermogenic in nature. So anybody who's ever woken up in the middle of the night with sweats knows that alcohol is thermogenic. So in fact, there's been some very interesting studies with heavy drinkers where they replace carbs with alcohol and they get lean.

30:35

Based on that thermogenic response, is that the mechanism? Interesting. Oh, yeah. In fact, I hate to say this because I know people are going to do it, but just lean protein, like lean anti-inflammatory protein like cod, something with a lot of omega-3s, something that's by its very nature anti-inflammatory, together with alcohol, you'll get lean.

31:04

But everybody knows heavy drinkers, people like winos. Everybody knows that wino in the back of the supermarket who just ripped the bone, right? Yeah. Yeah. Yeah. Well, it's because of the thermogenic nature of alcohol. Yeah. So by itself, it doesn't make you fat. But what it does do is that when you look at the conversion pathway to clear alcohol from the body, you have to convert it eventually into acetate to get rid of it.

31:33

And in order to do that, carb metabolism and fat metabolism takes a backseat. So carbs and fats will get stored in the presence of alcohol. And that's

31:43

That's where you get in trouble. That's where it gets skewed. A lot of wines now are really sugary and so you have an inherent problem because it's a high sugar wine, you got alcohol. And wherever you find carbohydrate together with alcohol, that's a problem. And fat too. But lean protein sources together with alcohol aren't really the problem that we think they are.

32:06

So that's one of the ways you begin to hack it is when you're going out and when you're drinking is just understanding what foods are complementary with alcohol. And so very lean protein sources, typically fish work really well. And then there are certain vegetables that also are very complementary. So asparagus and broccoli are the two that really stand out. Asparagus increases alcohol dehydrogenase.

32:32

and another enzyme. And then broccoli, actually, the sulfur-fermenting broccoli activates certain genes that detoxify alcohol, and you'll actually get an increase in the cytosol for alcohol enzymes. So broccoli is very good and very complementary with asparagus. And so those two together with lean proteins, and then it depends on the type of alcohol that you're taking in. So basically, the hard stuff is kind of more the go-to.

33:01

So, because it doesn't have any carbs or anything with it. Beer is kind of like a much harder road to hoe because you're dealing with all the carbohydrates in it. Although I'm sure the people at Guinness would argue differently. So, go ahead. I was going to say, I was thinking of one potential benefit of alcohol that I don't know if it's really explored or researched is the effect on…

33:25

gastric acid production like is it going to help with protein degradation through gastric acid secretion like is that one is there research around that at all or hmm trying to think

33:42

i'm trying to think if i've ever read that i i don't know i don't know that i've actually looked at that i guess it has this region and alcohol protein degradation i don't know i couldn't answer that one yeah yeah yeah a big big good thing to study up on yeah like ethanol itself like is it a

34:00

a secretor of gastrin or gastric acid and then potentially that's why you know people say drink have a bit of lean protein with your alcohol help that actually stimulates digestion i'm wondering if if there's a link there if it's influencing other gut um stomach hormones things like that well um what's interesting and what's interesting about it is you know you're getting you're getting um

34:32

you're getting short chain fatty acid production out of it. Uh, and so you're, um, you're getting, it's, you're going to get a couple of things out of alcohol. You're going to,

34:46

Number one, you're getting sort of the cousin of a ketone body and you're getting sort of these alterations in short-chain fatty acid production. And how those play out as a result of alcohol, I don't know that it's been totally studied. But those are things that get very interesting because it affects the liver and it affects…

35:09

It just affects things sort of in a different way. So yeah, that's a whole topic we could kind of get into, like, you know, whether or not you're getting like acetate in the liver and all that junk. Yeah, yeah. With, from my listeners, they may not know the three types of short-chain fatty acids, butyrate, acetate, and propionate. Most of the research, correct me if I'm wrong, is conducted on butyrate.

35:33

um or in terms of promoting beneficial effects on human health but i haven't actually personally explored any around acetate or propionate so you offer any like insights around those two short chain fatty acids

35:47

Yeah. Well, there are benefits to all three short-chain fatty acids, but the most important thing is sort of the ratios of the three. You kind of optimally need them in certain ratios. You don't want too much acetate. Too much acetate will give you fatty liver. And then with propionate, if you have too much propionate, you can get things like certain autoimmune issues. So it's…

36:14

There are definitely benefits to both the PNA and acetate, but…

36:20

probably the bigger picture is to look at the whole and it's really the ratios of all three that you want to be optimal. And when you get into that discussion, there are a number of different metabolic pathways to create the short chain fatty acids. So one metabolic pathway is fermenting fiber, another is fermenting proteins. And then within fermenting proteins, you have a couple of different pathways. You have a ketogenic pathway where you can ferment

36:47

uh short chain fatty acids from and so the various different pathways will produce different end products um and the best thing to say probably is that ultimately there needs to be a balance in the way that you're producing short chain fatty acids like like you don't want to do it exclusively too much in one thing although the optimal home is probably fermenting them from fiber um

37:13

But that doesn't mean that you can't prevent them from proteins and different meal patterns in protein. So you can use keto meal patterns or you can use like kind of overfeeding patterns, carnivore patterns, things like that. But it's just that ultimately that they have to balance out. You don't want to get too much of like acetate or propionate relative to butyrate would be the way that I would answer that.

37:34

Right. Awesome. Okay. So let's sort of delve into a little bit around fat loss. I know you've covered a little bit on something known as FGF21. So do you want to explore this as an enzyme? What is it?

37:51

Yeah. So I can never say this word every time I try and think. It's fibroblast. My tongue like ties up on it. Fibroblast growth factor 21, FTF21. Yeah. FTF21 is a, it's a hormone.

38:08

And we used to think that it was primarily a starvation hormone, a hormone involved as a reaction to starvation. But then it turns out that you also make it when you're feasting too. So really what it is, FGF21 is a stress hormone. And it's produced and it does a number of things. It helps in a starvation state. FGF21 does a number of things in terms of like

38:34

The way that fat is released in partition and drives feasting and drives hunger, it can drive a lot of things. It can make insulin work better. It does a whole bunch of things. What's notable about FTF21 is that when we shrink fat cells, we get a reduction in FTF21. And so I have a course that I've released called Immune-Centric Fat Loss, which deals one of the aspects of…

39:01

of fat loss that's ever really been dealt or accounted for is that when fat cells shrink, there's a whole list of mechanisms that are activated. And nobody's ever bothered to actually inventory what they are. And that's a problem because the vast majority of people that take any, it doesn't matter what it is, any program, they all regain it within five years. And it's because to a large degree, we're not inventorying what the mechanisms are that happen when fat cells shrink. We're not dealing with what's true

39:30

And so as a result, we're not getting the results that we want. When you begin to inventory what's true and you start to see that there's all these different hormones and mechanisms and genes, all these things are happening post-fat loss, just from the act of shrinking fat cells down. Well, one of those is FGF21, and that we need to increase FGF21 post-fat loss. And it's just something that really has… And when I ask that, I have no idea why that's never been accounted for. It just seems ridiculous to me. Yeah.

39:58

We should do things based on how things work, right? So anyways, FGF21 plus fat loss is something that we probably want to look to stimulate.

40:10

If we want to prevent weight regain, and there's some decent research on this too, like on basically getting FGF21 stimulated in the post-fat loss phase or in the maintenance phase. What a lot of people don't understand is that post-fat loss, you have a maintenance phase. And in that maintenance phase, there are very distinct sets of genes that turn on

40:29

And there's some good research that showed there's a cluster of genes, several dozen that activate in the post-fat loss phase. And they can very much dictate whether or not you're going to regain the weight or not. And that's just the genetic components. There's a number of other components. So the maintenance phase is a really critical piece of the equation that's never been accounted for ever, anywhere.

40:51

And FGF21 is kind of a big player in that. Interesting. Do we have any research around any botanicals, drugs, supplements, compounds, anything that can actually stimulate FGF21 at all? Well, metformin, one, but also berberine would be another one. Awesome.

41:13

Yeah. Bourbon and metformin, how odd. Yeah. And it's funny because they both share so many similar… This is what I find really fascinating. So many of these supplements and ergogenic aids and things, they all seem to…

41:27

tickle the same sort of pathway or they might like scrape the same sort of a lot of overlapping pathways which i find really fascinating so yeah that's that's that's new that's brand new to to me i've never heard of yeah this fibro fibroblast growth factor 21 um is is there much i was about to say is there research around this that you're excited to see more of or

41:51

Oh, yeah. It's a continuing field. Like FTF21 is…

41:58

has very much an evolving understanding on it. Like I said previously, just a few years ago, it was just thought to be the fasting hormone. But now we know that's not true. It's a stress hormone, which brings up a really good point that fat loss is inherently stressful on the body. It's stressful on the body. And so the body has a number of different stress responses.

42:22

because stress itself, particularly in fat loss, is coming from the fact that you're injuring the body at a cellular level. When you look at like, so here's your adipocyte, here's your ECM. What you're doing is you're ripping it away from the ECM when it shrinks.

42:42

Well, that's essentially like a tear. And so it's got to repair that. The ECM has to deform, has to try and, you know, has to pull this thing back, has to reach out to the out of the site, pull it back, has to shrink it. So there's all this stuff that's going on that mechanically speaking falls under what's known as mechanobiology. And under that, there's another sort of thing going on called mechanotransduction, which refers to signals and how signals propagate from mechanical forces.

43:09

And this affects body fat. It affects fat cells. It even affects whether or not they can release fat. Like literally, whether or not cells can release fat has a lot to do with the tension, tension within the cell. And you mentioned something, actually, you mentioned a really good point, which is how all these signals, these signal pathways converge.

43:33

What it really gets to, kind of big picture, is that growth…

43:41

Growing, perpetuation is the business of life. That is life. Okay? So there are things like the Hayflick limit where cells have 50, 60 allocations per cell. Well, growth is tightly, tightly, tightly regulated in the body. It has to be fine-tuned and tightly regulated. And it's like a road. It's like a toll road where every mile down that road, you're paying a toll to go down that road.

44:10

And kind of at the high level is really insulin and insulin's effect on a couple of key pathways, notably one called MATHK, mitogen-activated protein kinase.

44:25

And really, this is a pathway that controls the decisions that cells make about should we go forward and replicate and divide or should we not? Should we just kind of chill for a while and stay here?

44:40

And the big takeaway is for the listeners to begin to understand you can control that. You have control over that. You can turn that switch when you want to, and you can turn it off when you want to. So once you understand what turns that switch, which is the production of insulin, you can decide how fast you want to age. Yeah.

45:04

Yeah. I mean, that's, it's a great point there. And I'm glad you're really emphasizing this role and function of insulin outside the scope of just managing blood sugar, because it really has so many broad spectrum pleiotrophic effects that seem to be modulating aging, as you mentioned. So, yeah, I'd like to quickly touch on the AMPK versus mTOR

45:31

Yeah, because explain to my listeners how AmpK, AmpTor, and fasting and growth are all linked. So the best way to understand it is to understand two big concepts. It's that the production of energy and growth are one. They are the same thing. We think of them as different things, but they're not.

45:57

They're the same thing. So the body's ability to make energy is life itself. If every cell in your body stopped making energy right now, you'd be instantly dead. Instantly. Okay. So the body's ability to grow requires energy. It has to have energy to do that. In fact,

46:20

I make the point in my book that cells, we use the word cell, but really what you're looking at are computers. That's what they are. They're just a form of computer that's much more advanced than something we can associate as a computer because they incorporate energy production, they incorporate a 3D printer, and they incorporate information processing, and then structural integrity all into one thing. It becomes a single thing. But what they're doing is they're making decisions.

46:48

And they're making decisions on a regular basis, not just from computer code, but also from their environment. And so they're constantly making decisions about how to partition things. Well, the most important decision that a cell can make is to live or die. That's the most important decision. And that decision is based on energy production and power output. So within the cell, there's all these meters that essentially are always measuring power output. The power output in the cell gets too low

47:15

There are some backup measures. One of them is a protein that sits in the wall of cells. It's what's called a heterotrimeric protein, meaning a three-pronged protein.

47:28

And so one head is ATP, the next is ADP, the next is AMP. And so when energy gets down and hits this prong and this prong fires, a signal pathway fires. It sets a cascade of events in motion. And that cascade of events we call AMPK.

47:51

And what that does is it turns on a number of measures that change the way that we get energy. So it's very much like being on a ship.

48:03

and we're low on coal, so we're just gonna burn the deck chairs for a while, okay? We're gonna take all the spare furniture, a little spare part, let's just throw those in, okay? And in the process, the ship's lighter and it's cleaned up, kinda looks better. So, hey, there's a benefit to that, right? Well, that's kinda how AMK works. AMK is, it's a signal pathway when energy is low that turns off the process of growth.

48:31

Now, what we call mTOR really is a signal pathway and it is really referring to a series of kinases. That's what it's really referring to, serine 309 kinases. And this signal pathway is a pathway that essentially is tied to all of the body's signals to grow.

48:56

for cells to continue to advance down their cell cycle allotment and all these other signals that impinge upon growth. So the thing about what we call mTOR is that, again, kind of at the center of all this, you see energy and you see insulin driving all this. So that when energy is abundant,

49:21

Meaning when ATP is abundant, the mTOR and growth and all those things can go down that road. We can use up our primary fuel source. In other words, let's use the analogy of a car. The pistons can only go up and down so many times in that engine before there's wear and tear.

49:41

When we are activating amp K, that's like the electric drive on the car, the backup drive. And so the engine's not wearing out. But once fuel's abundant again, we can use the piston, and that's great. We can do a lot of things. We can really go for performance, but there's a cost. The cost is we're wearing out the engine when we use it. So all of the body's growth-centric pathways impinge upon these kinases that help release energy. And

50:07

and drive all the body's growth factors. So life and death, energy and growth, they're all kind of linked. And in that is…

50:19

In that, the body's sort of starvation pathways, which are AMPK and activation of very key proteins called the sirtuins, and salvage sort of pathways and cleanup pathways like ubiquitin, proteasome pathway, and autophagy, and all these things. All these other things activate when we're in a starved state. We use these words like fasting and time-restricted feeding. Our body doesn't understand what you're talking about. All it knows is just that starvation.

50:48

The body has defenses against starvation, but starvation serves a benefit too. It stops aging in a sense. So AMP-K and M4 are kind of these two ends of the seesaw. And kind of the cool thing is once you understand, once again, how to flip the switch, you can kind of, what I talked about in the very beginning, the power to control the body, you gain the power to control your rate of aging by understanding how to pedal these things.

51:15

Sorry, long-winded explanation. I hope that… No, that was beautifully summarized and very concise. Hopefully that makes sense to my listeners because I think they're critical points to understand. They're really critical energy sensors in the body. They mediate so many downstream biological functions. And for my listeners, just remember like, you know,

51:40

Stimulating mTOR is going to be achieved through high protein diet, increasing your caloric intake, whereas stimulating the mTA side of things is when there's a shortage of food supply, the body will stimulate that side, that pathway to preserve, maintain, and promote longevity. So really well put, Joel. I'd like to wrap up with one final question around the carnivore diet. Now,

52:09

I don't know if you've personally experimented with it. I'd just love to hear your opinions around, you know, maybe some pros and cons around the carnivore diet.

52:19

Yeah, I think the carnivore diet, first of all, there's a lot of, I think it's extremely useful. And I'm just after, I'm like a martial artist. I'm just looking for new techniques. Okay. So if you've got a way to kick that is fantastic, I want to learn it. Okay. But at the end of the day, I'm not relying on any one thing. I'm mixing them all into one thing so that whatever I'm presented with, I have a response for. Okay. That's the way that I'm approaching this.

52:49

So that being said, the carnivore diet kind of fits under the aegis of something I talk about in the book, which is the era of imbalance. And I make the point that we have gotten away from what's really true. We have, as a whole, believed something that's not true. We believe that we can obtain…

53:13

uh, health through imbalance. And that's kind of something to really think about because every school of thought today is telling you to imbalance your health inputs, you know, like, and they all fight with each other. So on the one hand, it's like, you know, meat's bad, meat's murder, uh, meat sucks, you know, uh, just eat plants and, you know, and then, and then keto and all these different schools. But when you look at it, when you look at the thing that we call disease, uh,

53:38

The one consistent thing that you find is that you cannot describe a disease without using the word imbalance or homeostasis, loss of homeostasis. All diseases are just an imbalance of something. And so we believe something that's not true, which is that we can obtain health through imbalanced inputs. And that's just going against the laws of physics in terms of how the body works. So there's always a short-term and a long-term

54:07

The short term is that you'll probably see a lot of benefits in the short term. And the carnivore diet is great. It's great for adding muscle. It's great for fat loss, probably heal your gut if you have issues temporarily. But over the long term, that's where things really play out. And what you're probably going to see over the long term, I would just begin by asking yourself, are there any known disease states that can come from an excess consumption of meat or protein? That's what I would ask.

54:35

And the answer to that is, yeah, absolutely. Yeah, colon cancer probably top of the list. Yeah, 100%. Well, are there any mechanisms that would substantiate that? Yes. I talk about them in my book. You have to understand that, you know, do bacteria like meat

54:54

Yeah. Right? Yeah. Leave a piece of meat out and watch what happens. Right? But the kind of bacteria that like meat are some of the nastiest bacteria known. I mean, the type of bacteria that want to ferment meat are some very nasty players, some very pro-carcinogenic players. And not just that, but

55:16

There are all kinds of mechanisms you can see, particularly when you get into the colon, where you can see an increase in pH, you can see things like N-glycol, neuraminic acid, you can see all these sort of oncogenic things that happen. If you do it too much, you need to do it too long. And then there are ways to offset that. So you add a little bit of fiber in with meat, you can push the pH of the colon back down, and you just see those risks go away. So I would say that…

55:41

over the long term that a lot of people would probably see, could in fact have a chance to see some health related issues from imbalancing too much, too much meat in the diet, too much protein in that way. Where in the short term, you'll probably see a lot of benefits. And it just gets to how the body really works. And the truth is that you can…

56:04

There isn't anything I can think of that if you do it to an imbalance that won't make you sick in some way. It's true of water. It's true of fiber. And yeah, it's true of meat too. So the highest truth of health is that balance…

56:19

uh rules the body and the imbalance inputs eventually will produce imbalance in the body this doesn't matter what it is you could take anything and imbalance it and eventually it's going to cause a problem so uh that's the way to explain it i think in 10 years we're going to look back on this era and kind of see like wow

56:36

yeah, how did we buy that? We were just kind of in balancing everything. And that really the real truth is that a healthy balanced diet always was the best answer. It's just, we'll be at a new level. We'll be at understanding that it's really meal sequencing and it's really like using foods functionally in these sequences. And that's kind of the next thing. So time will tell. Time will tell with the carnivore community.

56:56

Yeah, I think… I know, I mean, you've got a bunch of haters now. Yeah, but I think, like you said, like anything to an extreme is going to have some downstream consequence. And I think the one thing that they pull from is that, is there like literally one or two studies that they keep on drawing upon? Have you seen those like long-term carnivore diet studies? I think there's like one. What are they finding by long-term?

57:25

It was only conducted in like the sample size, I think it was like two participants. I'm not exactly sure. I'll have to double check. But yeah, I mean, it was basically illustrating zero effects on ill health. Like it just had no deleterious effects. What was the duration? What are they calling long-term? I think it was at least 30 years. I'll have to… Yeah. Well, first of all, that's…

57:54

I mean, that's just gibberish. I mean, there's been no formal… That's purely anecdotal reporting just put into or dressed up as science. That has nothing to do with anything. Look, I'm a fan of the carnivore diet as a protocol. There's a lot of great…

58:16

What I've been doing for a number of years is something more close to what I would call martial art. And it's just that when you begin to factor in what, when and how into anything, you'll find that there's a use for just about any eating protocol at a certain time in a certain way. And so carnivore diets are great. They're very functional. I just don't do them

58:39

I just don't do them long term and as a way of life. That's the only difference. But there's a lot of utility to it. So that's probably where we differ. Or rather, I would differ from a strong adherent. In fact, I'll probably call it Mark Bell. Yeah, I share a very similar stance in that regard. The one thing that really just frustrates me about what people say about

59:04

eliminating these polyphenols and oxalates. I understand that. I understand that can be toxic. But what about all the research that we have that demonstrates the beneficial effects of these polyphenols on these pathways we've just spoken about, like improving endothelial function, improving ENOS, like modulating ACE enzyme. These polyphenols are definitely having these biological effects that meat on its own just does not address.

59:34

Well, okay. In 2006, I wrote an article on grass-fed beef in an era when beef was vilified. And I referenced all the available literature which is coming out of Northern California, talking about the benefits of grass-fed meat. So I've been a long time adherent of meat as a superfood. And I still am. And it's part of my diet on a regular basis.

01:00:04

I think there is a… I'm speaking right now as a consumer who has done things for a lot of years. And…

01:00:14

What will happen is when you get to the end of a road, it takes a long time to find out what was really healthy. And you may not be happy with the answer doing something that you thought was healthy and it really wasn't. And the only person who's going to pay for it is you. But when you make a list of the 10 or 12 greatest superfoods, almost every one on that list comes from a plant.

01:00:39

Now, I would put salmon in there, I'd put grass-fed beef in there, but the majority of those are going to be plants. And that's because they're highly functional. And I don't get into this, meat's bad, plant's good. To me, again, I talk about this in the book and I just explained that that's one-dimensional baby talk from a generation or from an era that's dying.

01:01:02

It's from an era when we looked at these hyper-polarized extremes and we're really just doing simplistic talk about things. What I'm seeing is a new generation forming of people that are much more interested in a much more nuanced, more accurate conversation of how things work versus just getting into debating narratives and things like that. There are mechanisms that we can look at and identify that are highly beneficial in polyphenols and they're just healthy.

01:01:32

Yeah. So why ignore it? Yeah. I love meat. I love a good ribeye by itself. I mean, I love that. I'll do that several times a week. But so what? I mean, polyphenols are healthy. Yeah. Yeah. Joel, for my listeners, if they want to learn more about these books you keep mentioning and some of your other resources, where can they delve into all of your amazing resources?

01:01:56

Oh yeah. So the book is The Immunity Code and Veep Nutrition, veepnutrition.com. And then we have also the Immune-Centered Fat Loss Course there and other goodies. So yeah, I'd love to come on by. Awesome. Well, for those listening in, I'll make sure to link those in the show notes. You can check those out. That Immune-Centered Fat Loss Course, that to me is such a novel concept that really excites me that you're

01:02:24

tackling sort of addressing fat loss from such a unique angle a unique perspective I'm sure they've been green food would be very very proud of that concept because you know we both love that novel novel pathways which is cool yeah but Joel thanks so much for coming on the show man I've got one final question and that is basically

01:02:49

Just out of curiosity, is there one area within research that you're really excited to see more of? I think it probably has to do with, yeah, I'd like to see more on…

01:03:10

the long-term effects of ECM dynamics in different collagen proteins post-adipose remodeling. So when we remodel

01:03:25

our fat mass, um, different kinds of collagen fibers get, get put back in to the ECM. And, uh, it's, it's really difficult to appreciate what these things really are because the words don't describe, we use these words, collagen and fibers, but they're, that's not what they are. They're,

01:03:44

I can't even really… Just find an analogy for what these things are. It's like they're sort of like computational construction materials that talk back and forth to the cell. It's like a smart building where you have this ongoing dynamic sort of tensioning and all this crazy stuff happening. And I think it's a thing that's just in identity right now. So I think it's going to be really fascinating to see what

01:04:12

what comes down the line with that. Awesome. Okay. Well, hopefully once you find out more about that, you can probably share some educational content around that. So Joel, thanks so much. Thanks for letting me know it up today. Yeah, it was a lot of fun. I know my listeners are going to absolutely love this episode. So it'll be on across all platforms. I just want to say a massive thanks again, Joel.

01:04:39

Hey, thank you. This was fun. Sorry. And thanks for letting me just babble. I can see you coming back for a second episode. That's for sure. That would be fun. Awesome. Thank you everyone for joining in to today's episode. For in-depth show notes and lessons learned, visit nofilter.media forward slash boostyourbiology.

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