Artificial intelligence is not an autonomous existential threat. Intelligence-the ability to solve problems-is distinct from agency, the ability to set and pursue goals. AI systems exhiabit superhuman intelligence but remain entirely devoid of intrinsic agency. The true existential risk does not come from AI itself, but from humans wielding AI to manipulate perception at unprecedented scale. AI's extraordinary capacity to distort reality enables mass behavioral modification, culminating in an inevitable epistemic collapse. As synthetic content proliferates exponentially, the ratio of authentic to synthetic information trends toward zero. Centralized verification systems cannot contain this flood. The only viable defense is decentralized collective verification, as demonstrated by Wikipedia, X's Community Notes, Reddit's moderation, Stack Overflow's peer-review, and the scientific method itself. Humanity's collective intelligence, acting as a distributed neural network, is the only force capable of distinguishing reality from illusion. The existential threat posed by AI is human-driven. Its solution must be as well.

America's greatest existential threat is not external aggression—it is internal division. Democracy requires social cohesion and shared reality, both threatened by artificial intelligence. AI shatters common ground through individualized realities—whether deliberately weaponized by adversaries or amplified by profit-seeking algorithms. This fragmentation cripples cooperation, undermines governance, and destabilizes democracy. Empirical evidence confirms this pattern: polarization metrics worsen directly with AI-driven content consumption. Critics argue technological shifts have always prompted adaptation, not collapse. Yet AI differs fundamentally from past information revolutions in its personalization capacity and algorithmic opacity. Traditional governance cannot counter this threat alone. Proven solutions exist in decentralized community moderation systems already functioning at scale on platforms like Wikipedia and X. These systems, combined with mandatory content labeling and widespread digital literacy, create an immune response to misinformation. The American experiment has always been fragile. In the age of AI, its survival demands immediate action from government, technology companies, and citizens. This is not speculative futurism. It is today's clear and present danger.

Academia claims to sell knowledge, but knowledge is now free. If knowledge is free, universities cannot justify their existence by providing information alone. Therefore, they must sell something else: status.Universities no longer hold a monopoly on learning. The internet, AI, and open-access research have made high-quality education widely available at little or no cost. Yet, academia retains its power by maintaining a credential monopoly, reinforcing exclusivity, and controlling access to research funding and professional validation.This paper examines how academia transitioned from knowledge gatekeeper to status gatekeeper. It explores the historical role of universities, their resistance to disruptive change, and the structural incentives that prioritize prestige over accessibility. The conclusion is clear: higher education must evolve into an open, decentralized model or risk becoming obsolete.

Writing is not thinking-it is a tool for encoding and transmitting ideas. AI is not replacing thought; it is eliminating the inefficiency of manually translating thought into text, just as calculators removed the inefficiency of manual computation. Resistance to this shift is driven by cognitive inertia, the same reaction that met every past advancement in communication-from writing itself to the printing press to the word processor. The value of thought lies in the idea, not in the mechanics of its transmission.

I. INTRODUCTION GLP-1 receptor agonists (GLP-1s) have been widely adopted as a pharmaceutical treatment for obesity. They are marketed as a breakthrough intervention, with claims that they address one of the most pressing public health challenges of the modern era. However, while GLP-1s lead to weight loss, they do not necessarily restore metabolic health. This paper examines the role of GLP-1s within the broader chronic disease framework. It explores what these drugs do, what they do not do, and how they fit into the existing medical and pharmaceutical landscape. The goal is not to criticize or defend GLP-1s but to describe their function and limitations objectively. The central issue is this: obesity is a symptom, not the root cause of metabolic dysfunction. Effective long-term health solutions require addressing insulin resistance, mitochondrial function, and metabolic flexibility. Weight loss alone does not resolve these underlying problems. This paper will outline why GLP-1s are best understood as a tool for symptom management rather than a cure for metabolic disease. Understanding how GLP-1s fit within the broader system of chronic disease management provides insight into how medical treatments are developed, prescribed, and maintained. This paper will assess GLP-1s within that framework, showing how their use aligns with existing healthcare incentives and long-term treatment models. ------------------------------------------------------------------------ II. THE METABOLIC VS. OBESITY FALLACY Obesity is often framed as the core problem, but it is merely a visible symptom of deeper metabolic dysfunction. Metabolic health is not defined by body weight alone; it depends on the body’s ability to regulate energy, maintain insulin sensitivity, and efficiently adapt to different fuel sources. - Obesity is one possible outcome of metabolic dysfunction, but not the only one. - Weight loss does not guarantee metabolic restoration. - Thin individuals can have significant metabolic dysfunction. - Metabolic health is defined by functional energy regulation, not by body weight alone. Because obesity is easy to measure, it has become the primary target of pharmaceutical interventions. However, treating obesity without addressing the metabolic dysfunction beneath it results in temporary solutions rather than long-term health improvements. If core issues such as insulin resistance and mitochondrial dysfunction remain uncorrected, the underlying problem persists even if weight decreases. GLP-1s primarily act by reducing appetite, leading to lower food intake and subsequent weight loss. While this may improve certain health markers in the short term, it does not inherently resolve the physiological mechanisms driving metabolic disease. Studies show that metabolic benefits from GLP-1 therapy disappear after discontinuation, reinforcing that they manage symptoms rather than cure the underlying dysfunction. ------------------------------------------------------------------------ III. WHAT GLP-1S FIX (AND WHAT THEY DON’T) GLP-1 receptor agonists function by mimicking the incretin hormone GLP-1, which regulates appetite and insulin secretion. Their primary mechanism of action is appetite suppression, leading to reduced caloric intake and subsequent weight loss. However, weight loss alone does not equate to metabolic restoration. What GLP-1s Do - Suppress appetite, leading to lower food intake. - Improve short-term glycemic control by increasing insulin secretion. - Reduce body weight, alleviating some strain on the system. What GLP-1s Do Not Do - They do not restore insulin sensitivity - They do not fix mitochondrial dysfunction - They do not improve metabolic flexibility - They do not resolve chronic inflammation or hormonal dysregulation While GLP-1s lead to measurable improvements in body weight and short-term metabolic markers, their effects are largely symptomatic. The core metabolic dysfunction—dysregulated insulin signaling, impaired mitochondrial function, and systemic inflammation—remains unaddressed. GLP-1s temporarily improve glucose control and inflammation while in use, but they do not induce lasting metabolic adaptation. Once discontinued, these markers frequently return to pre-treatment levels, reinforcing their role as a symptom management tool rather than a curative intervention. A person on GLP-1s might eat less and lose weight, but their metabolic health remains fragile. This is why most patients regain weight after discontinuing treatment—the underlying system was never repaired. ------------------------------------------------------------------------ IV. THE HOLY GRAIL OF PHARMA GLP-1 receptor agonists are not just another drug—they represent the perfect pharmaceutical product from a business standpoint. Their financial success is driven by two key factors: the size of the potential customer base and the necessity for long-term use. The Massive Addressable Market The U.S. adult population is approximately 260 million, with 73% classified as overweight or obese. This means roughly 189.8 million individuals could be eligible for GLP-1 therapy. While not all will use these drugs, adoption rates will depend on medical eligibility, prescription trends, cost, and patient adherence. Projected Revenue Over the Next Decade The average annual cost of GLP-1 therapy is $14,453. If even 10-20% of eligible individuals remain on the drug long-term, the potential revenue is: (19 38 ) \times 14,453 \times 10 = \$2.7 \$5.5 \notag For context, the entire U.S. healthcare expenditure is around $4.3 trillion annually. Over a decade, GLP-1s alone could generate revenue comparable to the entire annual U.S. healthcare spend. This positions them as one of the most lucrative pharmaceutical products in history. To reinforce the scale of this opportunity, the revenue potential can be expressed as: \times = \notag In the case of GLP-1s, the combination of a vast potential customer base and exceptionally high lifetime revenue per user—due to the necessity for long-term treatment—creates an unprecedented market opportunity. This simple equation highlights why GLP-1 receptor agonists represent one of the most lucrative pharmaceutical products in history. The Ideal Pharmaceutical Product GLP-1s align perfectly with the pharmaceutical industry’s financial model because they offer: - A large and expanding customer base. - A treatment that requires lifelong adherence for sustained benefits. - Institutional and government reimbursement, ensuring steady revenue. A Perfectly Aligned Incentive System From a corporate standpoint, there is no better scenario. A single drug class that combines a high number of users with high lifetime revenue per user is the ideal pharmaceutical product. The incentives for GLP-1 expansion are therefore not just medical but economic: these drugs maximize profitability while fitting seamlessly into the chronic disease management model. The financial incentives of GLP-1s explain why pharmaceutical companies will continue investing heavily in expanding their use cases—not just for obesity, but for diabetes, cardiovascular risk reduction, and additional indications. This is not about bad intentions; it is about the natural optimization of the healthcare system’s economic structure. ------------------------------------------------------------------------ V. WHY GLP-1S FIT THE BUSINESS MODEL GLP-1s do not restore metabolic health; they create the appearance of it by inducing weight loss while leaving underlying dysfunction uncorrected. Weight loss is a visible change, but it does not equate to true metabolic function. This distinction is crucial because it explains why GLP-1s align so well with the existing chronic disease treatment model. GLP-1s vs. Bariatric Surgery – Management vs. Restoration GLP-1s function as cosmetic surgery for metabolism. They make the body appear healthier by reducing weight, but they do not fix the underlying dysfunction. The fundamental issues—insulin resistance, mitochondrial inefficiency, and metabolic inflexibility—remain uncorrected. Patients feel and look better in the short term, reinforcing the illusion that the problem has been solved. Unlike GLP-1s, which rely on continuous drug administration to sustain weight loss, bariatric surgery permanently alters gut hormones (GLP-1, PYY, ghrelin) and bile acid signaling, leading to sustained metabolic adaptation—even after weight stabilization. In contrast, bariatric surgery induces long-terbariatric surgery leads to sustained insulin sensitivity improvements, increased metabolic flexibility, and even diabetes remission. Unlike GLP-1s, which only work while actively taken, the effects of surgery persist even after the initial weight loss phase. The difference is clear: surgery rewires metabolism, while GLP-1s merely suppress appetite. The Business of Symptom Management The chronic disease business model ensures that solutions prioritize symptom management over actual resolution. The food industry creates metabolic dysfunction by flooding the market with ultra-processed, insulin-spiking foods. The pharmaceutical industry responds by developing drugs that treat the symptoms of this dysfunction without addressing its cause. The healthcare system benefits from managing chronic conditions rather than curing them. GLP-1s fit seamlessly into this structure. They reduce a symptom—obesity—but do not eliminate the metabolic dysfunction that drives it. As a result, they function as a long-term management tool rather than a curative intervention. This is not a failure of the pharmaceutical industry; it is a predictable outcome of how the healthcare system is structured. When economic incentives favor symptom management over disease resolution, treatments will naturally align with that reality. The goal is not to eliminate metabolic disease—it is to create a treatment model that ensures continuous patient reliance. ------------------------------------------------------------------------ VI. THE PEOPLE WITHIN THE SYSTEM GLP-1s are not the product of deception or malice. They exist because the system optimizes for treatments that align with its incentives. Everyone involved—pharmaceutical researchers, doctors, and patients—believes they are contributing to a meaningful solution. Pharmaceutical scientists develop drugs that effectively reduce weight and improve short-term metabolic markers. From their perspective, they are addressing a major public health issue. Doctors see weight loss, lower blood sugar levels, and improved patient outcomes. Within the framework they operate in, GLP-1s are a valuable tool. Patients experience significant benefits, including appetite suppression, weight loss, and improved health markers. However, these effects are drug-dependent. There is no orchestrated effort to mislead—each part of the system functions as designed. Pharmaceutical companies optimize for profitable, long-term treatments because that is how they sustain themselves. Doctors prescribe within their guidelines, which prioritize treating obesity as a primary metric. Patients seek solutions for weight loss, and GLP-1s provide a tangible result. A System That Rewards Management Over Resolution GLP-1s succeed within the system because they produce an outcome that aligns with measurable healthcare goals. However, the deeper issue remains: metabolic dysfunction is not being reversed, only managed. This is not a flaw of individual actors, but a reflection of how modern healthcare is structured. The pharmaceutical industry does not prioritize symptom management due to malice—it does so because the economic model incentivizes it. Doctors follow clinical guidelines that emphasize treating measurable outcomes like BMI and blood glucose. Patients, seeing tangible weight loss, believe they are improving their health. Each participant is optimizing within the system as it exists. Yet, despite good intentions at every level, the result remains the same: metabolic disease persists, and long-term pharmaceutical reliance becomes the default treatment strategy rather than true health restoration. ------------------------------------------------------------------------ VII. THE ONLY REAL SOLUTION IS METABOLIC RESTORATION GLP-1s offer a short-term intervention for obesity but do not restore metabolic health. They suppress appetite, leading to weight loss, but they do not correct insulin resistance, mitochondrial dysfunction, or metabolic inflexibility. As a result, they function as a management tool rather than a curative solution. It is psychologically comforting to believe that a simple injection or pill can solve this crisis. The idea of an easy fix is appealing. But the body is a complex system, and metabolic dysfunction cannot be reversed with a single pharmaceutical intervention. Weight loss is not metabolic health. GLP-1s alter body composition without fixing the underlying dysfunction. When patients discontinue GLP-1s, weight regain is common because the body remains in a metabolically compromised state. The healthcare system rewards symptom management, prioritizing measurable outcomes like weight loss over true metabolic restoration. GLP-1s and the Football Helmet Effect: A False Sense of Security The history of football helmets provides a perfect analogy for GLP-1s. Before helmets, players were more cautious, knowing that head impacts carried serious risk. But when helmets became standard, the perception of safety increased, leading to more reckless play and harder hits, ultimately resulting in more concussions and long-term brain injuries. The helmet didn’t eliminate harm—it masked the danger, encouraging behaviors that made injuries worse. GLP-1s function the same way. They give the illusion of metabolic health by facilitating weight loss, but the underlying dysfunction remains. This false sense of security can lead people to be more reckless with their diet and lifestyle, assuming the drug has “fixed” the problem. In reality, without addressing insulin resistance, mitochondrial health, and metabolic flexibility, the dysfunction persists beneath the surface. When patients stop the drug, the issue resurfaces, often worse than before. GLP-1s function much like wearing glasses for poor vision. Glasses correct your sight while you wear them, but once removed, your eyesight is exactly as bad as before. They don’t fix the underlying function of your eyes, just as GLP-1s don’t fix metabolic dysfunction—they only provide temporary symptom relief. Weight loss occurs while on the drug, but once stopped, the body returns to its previous metabolic state, often leading to weight regain and the re-emergence of insulin resistance and inflammation. The Only Path Forward: Fixing the System, Not the Symptom The only long-term solution is to address metabolic dysfunction at its root—insulin sensitivity, mitochondrial efficiency, and energy regulation. True metabolic restoration cannot be achieved through pharmaceuticals alone; it requires dietary and lifestyle interventions that realign with biological function. If the healthcare system does not shift its focus from symptom suppression to metabolic repair, the cycle of chronic disease management will continue. GLP-1s demonstrate how modern medicine approaches metabolic disease—not by fixing the system, but by managing a symptom. Until metabolic health is prioritized as the true goal, pharmaceuticals will remain a tool for temporary control rather than lasting change. This paper highlights how GLP-1s fit within the broader chronic disease system, but the actual solution is outlined in _The Chronic Crisis_, _Metabolic Overload_, and _Metabolic Eating_. These papers provide a complete framework for understanding the structural, biological, and behavioral corrections required to restore true metabolic function. ------------------------------------------------------------------------ KEY TAKEAWAYS - WEIGHT LOSS IS NOT METABOLIC HEALTH GLP-1s reduce weight, but they do not restore insulin sensitivity, mitochondrial function, or metabolic flexibility. - GLP-1 DEPENDENCE REINFORCES SYMPTOM MANAGEMENT Patients must remain on the drug to sustain results, as the underlying metabolic dysfunction remains unresolved. - THE HEALTHCARE SYSTEM PRIORITIZES MEASURABLE OUTCOMES OVER TRUE SOLUTIONS GLP-1s succeed because they produce weight loss, which is an easy-to-measure metric, even though deeper metabolic dysfunction persists. - PHARMA PROFITS FROM CHRONIC DISEASE MANAGEMENT, NOT RESOLUTION Long-term GLP-1 use aligns with the financial incentives of the pharmaceutical industry, which benefits from recurring prescriptions over permanent solutions. - THE REAL SOLUTION IS METABOLIC RESTORATION True health requires fixing insulin resistance, mitochondrial function, and metabolic flexibility, which cannot be achieved through pharmaceuticals alone. - THE PATH TO METABOLIC HEALTH IS OUTLINED IN THE FULL FRAMEWORK _The Chronic Crisis_, _Metabolic Overload_, and _Metabolic Eating_ provide the comprehensive roadmap to restoring metabolic function. ------------------------------------------------------------------------ FALSIFICATION CHECK As Richard Feynman famously stated: “It doesn’t matter how beautiful your theory is, it doesn’t matter how smart you are. If it doesn’t agree with experiment, it’s wrong.” The purpose of this section is to ensure that this framework adheres to that principle. A claim, theory, or model is only meaningful if it remains consistent with observable reality. This principle of falsification is the cornerstone of the scientific method, ensuring that only theories that withstand rigorous scrutiny remain accepted as valid explanations of reality. There are only two possible outcomes for any falsifiable claim: 1. FALSIFICATION: If a premise is contradicted by empirical observations, the framework must be revised or discarded. 2. PROVISIONAL ACCEPTANCE: If a premise cannot be falsified, it must be provisionally accepted as the best available explanation until such time that it can be falsified. The framework rests on the following premises, each of which must hold for the argument to remain valid: 1. GLP-1S DO NOT RESTORE METABOLIC HEALTH. Weight loss alone does not equate to metabolic function. If GLP-1s truly reversed insulin resistance, mitochondrial dysfunction, and metabolic inflexibility, long-term use would not be necessary. _Falsification:_ If long-term studies demonstrate that GLP-1s lead to sustained metabolic health improvements after discontinuation, this premise would be invalidated. 2. GLP-1S FUNCTION AS A SYMPTOM MANAGEMENT TOOL, NOT A CURE. If they reversed metabolic dysfunction, patients would not require lifelong use. _Falsification:_ If evidence emerged showing that GLP-1 users could discontinue treatment without regaining weight or experiencing metabolic decline, this premise would be disproven. 3. THE CHRONIC DISEASE MODEL INCENTIVIZES LONG-TERM PHARMA DEPENDENCY. The economic structure of healthcare prioritizes treatment over resolution. _Falsification:_ If a shift in healthcare policy or pharmaceutical research resulted in GLP-1s being prescribed as a short-term intervention with permanent metabolic restoration, this premise would be invalidated. Until one of these premises is disproven, the framework must be provisionally accepted. This ensures that the structure of knowledge remains dynamic—always open to challenge, yet stable when no contradictions exist. Science is not about defending ideas—it is about refining understanding. If this framework is falsified or refined, that is not a loss but a gain. I will be the first to celebrate, because it means we will have advanced our knowledge even further.

For decades, cancer biology has grappled with the paradox of diverse cancers exhibiting similar hallmark behaviors and the persistent challenge of therapeutic resistance. This paper defines cancer as an entropic process—a system where mutation-driven disorder competes with repair mechanisms. By formalizing DNA entropy as a quantifiable metric, we establish a predictive model for cancer progression.This framework explains how hallmark behaviors predictably emerge from corrupted genetic instructions and why resistance arises when therapies target downstream effects rather than root causes. By identifying DNA repair as a fundamental intervention point, it offers testable predictions about cancer progression and strategies to mitigate entropy accumulation. Bridging theoretical innovation with modern technologies such as CRISPR, AI-driven genomic analysis, and molecular monitoring, this framework provides a comprehensive foundation for advancing cancer research and developing durable therapeutic strategies. 

The modern public health crisis is not an accident—it is the inevitable outcome of a system designed for profit, not health. The food industry, optimizing for efficiency and revenue, has transformed the global diet into one dominated by ultra-processed foods. Meanwhile, the healthcare industry, financially structured around disease management, thrives on chronic illness rather than prevention. The result is not a malfunction—it is the system working exactly as it was designed to.When any system is forced beyond its tolerances, failure is inevitable. The biological consequences—obesity, type 2 diabetes, cardiovascular disease, neurodegeneration—are not separate failures. They are the same failure state, playing out in different tissues.This paper reveals how economic structures, financial incentives, and policy decisions have aligned to create an environment where disease is the default outcome. It systematically dismantles the idea that these conditions are a matter of personal responsibility or genetic destiny. They are not anomalies—they are engineered results.This paper is Part 1 of a three-part series. Part 2, Metabolic Overload, details the biological consequences of this system. Part 3, Metabolic Eating, presents the necessary correction—how to realign nutrition with biological function to prevent systemic metabolic failure.

The human metabolism evolved under conditions of scarcity—finely tuned for whole foods, intermittent fasting, and rare glucose surges. The modern diet—dominated by ultra-processed foods and relentless carbohydrate exposure—overwhelms this system, forcing it into continuous metabolic stress. The question is not why metabolic disease is rising, but why we would expect anything else.When any system is forced beyond its tolerances, failure is inevitable. The biological consequences—obesity, type 2 diabetes, fatty liver disease, cardiovascular disorders, neurodegeneration—are not separate conditions. They are the same failure state manifesting in different tissues, at different speeds.This paper exposes how modern diets systematically override metabolic regulation, pushing the body into a state of perpetual dysregulation. It dismantles the myth that these conditions are personal failings or genetic inevitabilities. They are not anomalies—they are engineered outcomes.This paper is Part 2 of a three-part series. Part 1, The Chronic Crisis, details the structural incentives driving the modern health crisis. Part 3, Metabolic Eating, presents the necessary correction—how to realign nutrition with biological function to prevent systemic metabolic failure.

Modern eating habits are fundamentally misaligned with human biology. For most of history, food availability was inconsistent, and the body evolved to function efficiently through alternating periods of eating and fasting. Today, the prevailing norm of constant food intake—three meals a day plus snacks—contradicts these evolutionary mechanisms, forcing the body into a state of continuous metabolic stress.This paper presents Metabolic Eating: Pause. Prioritize. Protect., a framework designed to realign eating patterns with human physiology.Pausing between meals allows insulin levels to drop, enabling fat metabolism and restoring hunger regulation.Prioritizing protein and fat ensures stable energy and nutrient sufficiency.Protecting against metabolic stress involves consuming carbohydrates in a way that prevents insulin spikes and energy crashes.This framework is not a diet, nor is it a form of restriction. It is a structured approach to eating that works with the body rather than against it—promoting metabolic stability, sustained energy, and long-term health by aligning nutrition with biological design.This paper is Part 3 of a three-part series. The first two papers—The Chronic Crisis and Metabolic Overload—exposed the systemic and biological failures that have led to widespread metabolic disease. This paper presents the necessary correction: a structured approach to eating that realigns with human physiology rather than contradicting it. This is not a diet, nor is it restriction. It is the biological solution to an environment that has already failed.

Humanity's historical trajectory has been defined by an unbroken expansion of agency—our increasing ability to control our environment, movement, and destiny. This paper argues that the logical culmination of this trend is the development of mobile world-systems—self-sustaining, navigable civilizations capable of steering their own cosmic trajectory.Current space expansion strategies remain base-centric, relying on fixed planetary outposts that are constrained by resource dependence, static positioning, and vulnerability to external threats. In contrast, mobile world-systems eliminate these limitations by combining the resilience of natural ecosystems with the adaptability of engineered environments. This framework introduces the Cosmic Agency Ratio, a quantitative model demonstrating that human survival depends on the continuous increase of control over our environment. We argue that intermediate states—partial agency without full cosmic mobility—are inherently unstable over long timescales, leaving civilizations vulnerable to existential threats. The only sustainable outcome is full agency: the ability to dynamically navigate space rather than being bound to planetary fate.By synthesizing technological, societal, and philosophical imperatives, this paper presents mobile world-systems as not just a possibility, but an evolutionary necessity. The choice is clear: humanity can either remain passive passengers on a drifting planet, or seize control of its cosmic trajectory and take the helm of its own future.

The Black Swan theory mistakes gaps in knowledge for inherent randomness. "Unpredictable" events are not cosmic anomalies but reflections of observer ignorance. This paper introduces the Blind Turkey Principle, demonstrating that unpredictability is not a feature of reality but a failure to recognize system drivers. By analyzing historical case studies, we show that Black Swans dissolve when viewed with sufficient understanding. The illusion of unpredictability stems not from the events themselves but from the limits of the observer’s knowledge. True resilience is not about bracing for chaos but eliminating ignorance—transforming Black Swans into White Swans through directional mastery.

Modern science excels at pattern recognition but frequently confuses statistical significance with truth. The precision-scope trade-off forces researchers into a dilemma: precise but impractical studies or broad but causally weak ones. As data scales exponentially, spurious correlations proliferate, exacerbating the reproducibility crisis. To restore credibility, science must move beyond statistical detection and adopt frameworks that prioritize coherence and causal structure.